medoharatwa#dg14 gdg

EVALUATION OF MEDOHARA (HYPOLIPIDAEMIC)

EFFECT OF CHITRAKA (PLUMBAGO ZEYLANICA LINN.)

– AN EXPERIMENTAL STUDY

By:

MUKTAYAKKA ARALI

Dissertation submitted to the

Rajiv Gandhi University of Health Sciences, Karnataka, Bangalore

In partial fulfillment of the requirements for the degree of

AYURVEDA VACHASPATI M.D.

IN

DRAVYAGUNA

Under the Guidance of

Dr. KUBER SANKH M.D. (Ayu)

And Co-guidance of Dr. SHASHIKANTH B. NIDAGUNDI

M.D. (Ayu)

DEPARTMENT OF DRAVYA GUNA POST GRADUATE STUDIES & RESEARCH CENTER

SHRI D.G. MELMALAGI AYURVEDIC MEDICAL COLLEGE, GADAG - 582103

2006-2009

Ayurmitra

TAyComprehended

D.G.M.AYURVEDIC MEDICAL COLLEGE

POST GRADUATE STUDIES AND RESEARCH CENTER

GADAG - 582 103

This is to certify that the dissertation “Evaluation of medohara

(hypolipidaemic) effect of Chitraka (Plumbago zeylanica Linn.) – An experimental

study” is a bonafide research work done by Muktayakka Arali in partial fulfillment of

the requirement for the post graduation degree of “Ayurveda Vachaspati M.D. (Dravya

Guna)” Under Rajeev Gandhi University of Health Sciences, Bangalore, Karnataka.

Dr. Kuber Sankh

M.D. (Ayu)

Guide

Asst. Professor

Dept of Dravya Guna

DGMAMC, PGS&RC, Gadag

Date:

Place: Gadag

Dr. Shashikanth B. Nidagundi

M.D. (Ayu)

Co-guide

Lecturer

Dept of Dravya Guna

DGMAMC, PGS&RC, Gadag

Date:

Place: Gadag

J.S.V.V. SAMSTHE’S

D.G.M.AYURVEDIC MEDICAL COLLEGE

POST GRADUATE STUDIES AND RESEARCH CENTER

GADAG, 582 103

Endorsement by the H.O.D, principal/ head of the institution

This is to certify that the dissertation entitled “Evaluation of medohara


study” is a bonafide research work done by Muktayakka Arali under the guidance of

Dr. Kuber Sankh M.D. (Ayu), Asst. Professor, Dept of Dravya Guna, in partial

fulfillment of the requirement for the post graduation degree of “Ayurveda Vachaspati

M.D. in Dravya Guna” Under Rajiv Gandhi University of Health Sciences, Bangalore,

Karnataka.

.

(Dr. G. B. Patil)

Principal,

DGMAMC, PGS&RC

Gadag

Date:

Place: Gadag

(Dr. G. V. Mulagund)

Professor & HOD

Dept. of Dravya Guna

DGMAMC, PGS&RC

Date:

Place: Gadag

Declaration by the candidate

I here by declare that this dissertation / thesis entitled “Evaluation of medohara


study” is a bonafide and genuine research work carried out by me under the guidance of

Dr. Kuber Sankh M.D. (Ayu), Asst. Professor, Dept of Dravya Guna, DGMAMC,

PGS&RC, Gadag.

Date: Signature of the candidate

Place: Gadag (Muktayakka Arali)

© Copy right

Declaration by the candidate

I here by declare that the Rajiv Gandhi University of Health Sciences, Karnataka shall

have the rights to preserve, use and disseminate this dissertation/ thesis in print or

electronic format for the academic / research purpose.

Date:


© Rajiv Gandhi University of Health Sciences, Karnataka

i

ACKNOWLEDGEMENTS

Any research is not an individual effort. It is a contributory effort of many hearts,

hands and heads. I am very much thankful to the subjects of this study.

I am extremely happy to express my deepest sense of gratitude to my respected

guide Dr. Kuber Sankh, M.D. (Ayu) for having inspired me in selecting the subject and

for his valuable guidance at every stage in preparing the dissertation.

I am grateful to Co-guide Dr. Shashikanth B. Nidagundi, M.D. (Ayu) for his

valuable suggestions, constant encouragement and for kind co-operation at all levels of

my work.

I express my gratitude to Dr. G. V. Mulagund, Professor and H.O.D for his advice

and encouragement in every step of this work.

I am sincerely grateful to Dr. G. B. Patil, Principal, for his encouragement and

providing all necessary facilities for this research work.

I offer my sincere thankas to Dr. G. S. Hiremath, Proffessor and HOD, Dept of

Dravya Guna, DGMAMC, Gadag for their kind suggestion and co-operation.

I extend my gratitude to Dr. Purushottamacharyulu, Dr. P. Shivaramudu,

Dr.Suresh Babu, Dr. K.S.R. Prasad, Dr.M.C. Patil, Dr. K. S. Paraddi, Dr. U. V. Purad,

Dr. R.V. Shettar, Dr. G. Danappagoudar, Dr. S. N. Belawadi, Dr. Samudri, Dr. J. G.

Mitti, Dr. Yasmin A.P, Dr. B.G .Swami, Dr. Veena. Kori and Dr. Yerigeri, R.M.O.

DGMAMC, Gadag.

I am especially thankful to Mr. Manjunath K. P., Mr. Vishwanath Swamy, and Mr.

Shivakumar Inamdar, Dr Ashok B. K., Mr. Suresh Huggishettar and Mr. Girish for their

heartful cooperation, timely help and advice.

I express my immense gratitude to Shri. V. B. Mundinamani (librarian) and Mr.

Shyavi and Mr. Kerur for facilitating me in collection and production of my thesis.

ii

I am at a loss of words while thanking my beloved parents Shri Veeranna Arali and

Smt. Akkamahadevi V. Arali and my dear husband Mr. Danesh Kendur and his family

members for all the love, affection and efforts for my progress and success. I am

extremely happy to express my deepest sense of gratitude to my all uncles and aunties.

I am extremely happy to express my heartfelt gratitude my beloved daughter

Sanjana and sisters, Uma, Pankaja, Nirmala and my brother Sharanabasava for constant

help and encouragement to move ahead.

I take this moment to express my thanks to my senior friends Dr. Shivaleela

Kudari, Dr. Ashwini Vastrad, Dr. Shalini Sharma, Dr. V. M. Kataraki, Dr. Rudrakshi, Dr.

Shivaleela Kalyani, Dr. Kamalakshi for their support and advice.

My in depth regards to my friends Dr. Savitha Bhat, Dr. Jaya, Dr. Kalavati D. P.

Dr. Vijayalaxmi, Dr. Mukta Hiremath, Dr. Veena. Jigalur, Dr. Anupama, Dr. Kavitha, Dr.

Sarvamangala, Dr. Prasanna Joshi, Dr. Sanjeeva, Dr.Neeraj, Dr. Adarsha, Dr. Nataraja,

Dr. Udaya, Dr. Shaileja, Dr. Ravi, Dr. Shivakumar, Dr. Asha Maradka, Dr. C.C.

Hiremath, Dr. S. B. Rotti, Dr. Bhopesh, Dr Deepa T. for their support and cooperation.

I express my immense thanks to Prabhu and Shettyappa Gouda, attenders dept of

Dravya Guna for their cooperation during the experiment.

I pay my tributes to the souls of all the animals which were sacrificed for the sake

of my work.

I would like to express my cordial thanks to all those who helped me directly or

indirectly in this work.

Date:


iii

ABBREVIATION

A. Hru – Ashtanga hrudaya

A. San – Ashtanga sangraha

AK –Amarakosha

API -Ayurvedic Pharmacopeia of India

BPN -Bhavaprakash Nighantu

Bhai. Ra -Bhaishajya Ratnavali

CD -Chakradatta

Cha.sa -Charaka samhita

DN - Dhanvantari Nighantu

KN -Kaiyadeva Nighantu

MN -Madanapala Nighantu

Mah. N – Mahaushadha Nighantu

NA -Nighantu Adarsha

PVS - P.V. Sharma

RN -Raja Nighantu

SGN -Shaligrama Nighantu

Su.sa -Sushruta samhita

VM – Vrunda Madhava

Sthanas:

Chi -Chikitsa sthana

Su -Sutra sthana

Ut -Uttaratantra

Ka -Kalpa sthana

Sha -Shareera sthana

Ni -Nidana sthana

Vi -Vimana sthana

iv

ABSTRACT OF

“EVALUATION OF MEDOHARA (HYPOLIPIDAEMIC) EFFECT OF

CHITRAKA (PLUMBAGO ZEYLANICA LINN.)

– AN EXPERIMENTAL STUDY”.

The objective of this study was to evaluate the medohra (Hypolipidaemic) effect

of Chitraka (Plumbago zeylanica Linn.) in alcoholic extract and in churna form in

glucocorticoid induced hyperlipidaemia. Hydrocortisone was (10mg/kg/day/i.p)

administered for two weeks to albino rats to increase the serum lipid levels. Alcoholic

extract churna of Chitraka was then administered in a dose of 200mg/kg/day/p.o and

180mg/kg/day/p.o respectively for four weeks. Atorvastatin was taken as the standard

drug at the dose of 5.5mg/kg/day/i.p. Chitraka, both in alcoholic extract and churna form

had significantly lowered the levels of cholesterol, triglycerides, LDL, VLDL and

increased HDL levels in glucocorticoid pre-treated groups. It was also effective in

reducing hyperglycemia, which was also induced by hydrocortisone. It also reduced

tissue lipid content of liver and regressed atheroma and plaque formation in aorta. The

present study indicates that, Chitraka alcoholic extract and churna in a dose of

200mg/kg/day/p.o and 180mg/kg/day/p.o respectively, has significantly reversed the

hyperlipidaemia induced by glucocorticoid. This suggests need for a further in depth

evaluation.

Key words: Chitraka, Hyperlipidaemia, Medohara, Hypolipidaemic, Glucocorticoid.

v

INDEX OF

“EVALUATION OF MEDOHARA (HYPOLIPIDAEMIC) EFFECT OF

CHITRAKA (PLUMBAGO ZEYLANICA LINN.)

– AN EXPERIMENTAL STUDY

CHAPTER CONTENT PAGES

1 Introduction 1- 3

2 Aims and Objectives 4

3 Review of literature

- Drug review

- Disease review

5 – 37

38 - 68

4 Materials and Methods 69 - 82

5 Observations and Results 83 – 107

6 Discussion 108 – 115

7 Conclusion 116 -117

8 Summary 118 -119

9 Bibliographic References 120 -130

vi

LIST OF TABLES

Table 1: Drug review

Table No Title of Table Page No

1.1 Gana and varga of Chitraka according to different classics 7

1.2 Synonyms of Chitraka 8

1.3 Vernacular names of Chitraka 10

1.4 Rasapanchaka of Chitraka according to different classics 12

1.5 Karmas of Chitraka according to different classics 13

1.6 Rogaghnata of Chitraka according to different classics 14

1.7 Vishishta yogas of Chitraka 16-18

Table 2: Disease review

Table No Title of Table Page No

2.1 Clinical features of medoroga according to different authors 44

2.2 Normal serum lipid values 49

2.3 Characteristics of lipoprotein 59

2.4 Fredrickson’s classification of hyperlipoproteinemias 66

Table 3: Materials and methods Table No Title of Table Page No

3.1 Protocol of experiment 82

vii

Table 4: Observations and results Table No Title of Table Page No

4.1 Physico chemical values of Chitraka 83

4.2 Phytochemical analysis of Chitraka 85

4.3 Results of TLC 87

4.4 Master chart 90

4.5 Parameter 1.1 Values of Total cholesterol of all the groups 91

4.6 Summary of Data 91

4.7 ANOVA Table 92

4.8 Parameter 1.2 values of Triglyceride of all the groups 92


4.10 ANOVA Table 93

4.11 Parameter 1.3 Values of HDL cholesterol of all the groups 94


4.13 ANOVA Table 95

4.14 Parameter 1.4 Values of LDL cholesterol of all the groups 96


4.16 ANOVA Table 97

4.17 Parameter 1.5 Values of VLDL cholesterol of all the groups 97


4.19 ANOVA Table 98

4.20 Parameter 1.6 Values of serum glucose of all the groups 99


4.22 ANOVA Table 100

4.23 Comparison of mean values of lipid levels between normal 101

viii

control and hyperlipidemic control groups

4.24 Comparison of mean values of lipid levels in between

hyperlipidemic control and alcoholic extract treated groups.

101


hyperlipidemic control and churna treated groups.

102


hyperlipidemic control and standard drug treated groups.

102

4.27 Comparison of mean values of lipid levels in between normal

control and churna to normolipid groups.

103


hyperlipidemic control and alcoholic extract, churna and standard

drug treated groups.

103

4.29 Mean of all the groups for lipid levels 104

4.30 Mean of all the groups for serum glucose 105

LIST OF GRAPHS

Graph No Title of Graph Page No

1. Mean values of Total cholesterol of all groups 91

2. Mean values of Triglyceride of all groups 93

3. Mean values of HDL-C of all groups 95

4. Mean values of LDL-C of all groups 96

5. Mean values of VLDL-C of all groups 98

6. Mean values of Serum glucose of all groups 100

7. Comparison of mean values of lipid levels between normal


101

8. Comparison of mean values of lipid levels in between


101

ix



102



102

11. Comparison of mean values of lipid levels in between normal


103


hyperlipidemic control and alcoholic extract, churna and

standard drug treated groups.

103

LIST OF PHOTOGRAPHS

Plate No Title of the photograph

1 Fig 1- Chitraka (Plumbago zeylanica Linn)

Fig 2 – Inflorescence of Chitraka

Fig 3 – Root of Chitraka

2 Fig 4 – Dry root of Chitraka

Fig 5 – Coarse powder of Chitraka

Fig 6 – Fine powder of Chitraka

Fig 7 – Soxhlet extraction

Fig 8 & 9 – Alcohol extraction

3 Fig 10 – Weighing of albino rat

Fig 11 – Albino rats in the cage

Fig 12 – Intra peritoneal route of administration

Fig 13 – Oral route of administration

4 Thin layer chromatography

5 Histopathology of liver

6 Histopathology of aorta

Introduction...

Hypolipidaemic effect of Chitraka 1

INTRODUCTION

Cardiovascular diseases with an incidence of approximately 50% are the main

cause of death in most advanced countries 1. The disease burden contributed by

cardiovascular diseases has been increasing in the developing world also. The World

Health Organization (WHO) estimates that every year 12 million people worldwide die

from cardiovascular diseases, with most of them being from the developing world 2.

The underlying primary cause of cardiovascular disease is believed to be

atherosclerosis, a progressive multifactorial disease of the arterial wall 3, 4. Central to the

pathogenesis of atherosclerosis is deposition of cholesterol in the arterial wall 5.

Previously considered a disease of the affluent, the past three decades have seen

considerable decline in the incidence and prevalence of atherosclerotic coronary artery

disease in the industrialized western world; whereas at the same time this problem is

assuming epidemic proportion in the developing world 6.

Coronary artery disease among Asian Indians has been found to be more severe,

diffuse and associated with serious complication and increasing mortality at a younger

age 7. By 2020 it is estimated that it will be the major cause of death in all regions of

world 8.

CHD is the number one killer among the diseases and it accounts for 37% of adult

deaths in the US every year 9. In India; persons suffering from the CHD are doubled in

the last 20 years. In South India, CHD incidences are 7.4% in rural area and 13.9% in

urban area, which is higher than north India (Rural- 3% and urban 9.7%). Mortality from

cardiovascular disorders in India is 430/100000 in both sexes and in males it is 460

whereas in females it accounts for 400/100000 deaths per year 10. It has been predicted

Introduction...


that cardiovascular diseases will be the most important cause of mortality in India by year

2015 11.

Wealth of evidence from epidemiological, clinical and experimental studies has

established the association between hyperlipidaemia and atherosclerosis,

hypercholesteraemia is clearly a risk factor. Of the lipoproteins, it is the LDL which is the

most atherogenic, where as HDL offers a protective effect and helps in removing

cholesterol from the arterial wall 12. The risk of IHD in individuals with

hypercholesterolemia is about thrice as great as in those with normal plasma cholesterol

levels 13.

It is emerging as major health problem in the modern era as it (Hyperlipidaemia)

leads to coronary artery disease, myocardial infarction and cerebrovascular accidents.

Hyperlipidaemia is an important, yet modifiable risk factor of all lipid

abnormalities. Thus, it has been suggested that reduction of plasma lipid levels either by

dietic restriction or by drugs may prevent the development of atherosclerosis or arrest its

progress. Studies have shown that a reduction in plasma cholesterol does infact reduce

the risk of myocardial infarction 14. Overall, 1% reduction in plasma cholesterol

concentration in middle-aged men reportedly results in 2% reduction in the incidence of

CHD 15.

In Ayurveda, there is no direct reference of a single disease entity that can be

directly correlated with the hyperlipidaemia. Moreover different scholars have different

opinions about the nearest possible disease. Most of them have considered

hyperlipidaemia under the heading of Medoroga.

Introduction...


Purpose of the study:

The available drugs like statins, fibrates and nicotinic acid, though very effective,

have a spectrum of adverse effects and are costly 16. Although the well known

hypolipidaemic agent “statin therapy” reduces the mortality and morbidity associated

with coronary artery disease, most of them don’t achieve the LDL cholesterol level;

besides, it also has a lot of side effects like increased lithogenecity of bile, nausea,

abnormal liver function and myosytis.

In classics Chitraka is highly valued for its lekhana and medohara action.

Medoroga being Vatakapha dosha predominant disease, the drugs which are having Vata-

Kaphahara properties, are mainly used. Chitraka which is having Katu rasa, Ushna

veerya, Katu vipaka and Vata-Kaphahara properties 17 used to treat it.

In the present context in spite of various existing hypolipidaemic drugs there is

necessity of still better, safe and effective hypolipidaemic drugs. Again Chitraka is easily

available and cost effective drug.

So with due consideration to above reasons, the present study was taken up to

confirm experimentally, the hypolipidaemic effect of Chitraka.

Aims and objectives…


AIMS AND OBJECTIVES OF THE STUDY

1. To carry Preliminary Phytochemical investigations of Chitraka (Plumbago zeylanica

Linn.) including thin layer chromatography (TLC).

2. To evaluate the medohara (Hypolipidaemic) effect of Chitraka using the

glucocorticoid induced hyperlipidaemic experimental model.

3. To evaluate the action of alcoholic extract of Chitraka on hyperlipidaemic animals.

4. To evaluate the action of Chitraka churna on hyperlipidaemic animals.

5. To evaluate the action of Chitraka churna on normolipid animals.

6. To compare the action of test drug in alcohol extract and in churna form along with

hyperlipidaemic control and standard drug treated groups.

7. To evaluate and compare the histopathological changes of liver and aorta samples in

between the groups.

Drug review…


DRUG REVIEW Historical aspect of drug:

Veda: No references were found regarding the drug, Chitraka in the Veda.

Purana: Not found any references of Chitraka in Purana.

Samhita kala 18: We find various references in samhita period regarding varieties,

preparations that are indicated in many diseases.

Charaka samhita: Acharya Charaka first recorded therapeutic use of Chitraka. He

described the same drug widely in 168 different conditions by two synonyms. Among

these synonyms, Chitraka is repeated for 165 times & Agni is repeated for three times.

Sushruta samhita: Sushruta used it in 99 various conditions using synonyms viz,

Chitraka repeated for 85 times, Agni for 6 times, Hutabhuk for 3 times, Hutashan for 2

times and Hutash for 3 times.

Ashtanga Hrudaya: Chitraka has been mentioned 104 times in different preparations.

Here Chitraka has been referred by three synonyms viz, Chitraka for 67 times, Agni for

27 times and Agnika for 10 times.

Kashyapa samhita: Kashyapa recorded many uses of Chitraka especially in Balagraha

chikitsa, Grahabaadhaa chikitsa, Udavarta chikitsa, Rajayakshma chikitsa etc.

Sharanghadhara Samhita: Sharanghadhara used the Chitraka in different preparations

like Kwatha, Choorna, Asava etc according to different diseases viz, Udara roga, Shotha,

Pinasa, Kshaya etc.

Vangasena: Vangasena described it in the management of Medoroga, vatarakta,

Udararoga, Shotha etc.

Bhavaprakasha: Bhavamishra has mentioned it for the treatment of different diseases

Drug review…


like Grahani, Arsha, Pandu, Rajayakshma, and Kasa.

Chakradatta: Chakrapaani, advocates its use in Sleepada, Dadru, Nasaarsha, Galagraha

etc.

Amarkosha 19: Chitraka is mentioned in Vanaushadhi varga of Amarkosha-2/4/80.

Kautilya Arthashastra 20: Chitraka is mentioned in Kautilya Arthashashtra, while

explaining Asavasambhara dravya in 29th patha and in 33rd patha it is mentioned while

explaining useful Kalka sambhara dravya in the preparation of Sura for the King. (Kau.

Arth.Adhi.-2, Adhy-25, Prakarana-42, Patha- 25 & 33)

Nighantu kala: In the Nighantu Kala, Chitraka is explained with a variety of synonyms

and its Gunakarmas.

Adhunika kala: Acharya Mahendrakumar shastri in his Brihat Dravyagunadarsha,

Ramsusheel Sharma in his Vanaushadhi nidarshika have described Chitraka along with

its three varieties. It is also described in Dravyaguna vignana written by Vd. P.V.

Sharma, Dr. J. L. N. Shastri, Dr. G. Pandey and in Data base on medicinal plants Vol – I,

Wealth of India Vol -VIII.

Modern botanical texts and various flora have identified Shweta Chitraka

to Plumbago zeylanica, Rakta Chitraka to Plumbago rosea (Syn. P.indica Linn) and that

of Neela chitraka to Plumbago capensis.

Drug review…


Gana and varga:

Classification according to different classics:

Sl.No. Different authors Gana / Varga

1. Charaka samhita Lekhaneeya Dashemani, Bedhaneeya Dashemani,

Deepaneeya Dashemani, Triptighna Dashemani,

Arshoghna Dashemani, Shoolaprashamana Dashemani

& Katuskandha.

2. Sushruta samhita Aragvadhadi gana, Varunaadi gana, Mushakakadi

gana, Pippalyadi gana, Mustadi gana, Amalakyadi

gana, Veerataraadi gana.

3. Ashtanga sangraha Aushadi Varga,Soshanadi Gana, Vamaka Gana,

Aragwadhadi Gana, Mushkakadi Gana, Vatskadi Gana,

Mustadi Gana.

4. Ashtanga Hridaya Aragvadhadi gana, Mushkadi Gana, Mustadi

Gana,Varunaadi gana.

5. Dhanwantari Nighantu Shatapushpaadi varga

6. Maadhava dravyaguna Shaaka varga

7. Madanapala Nighantu Shuntyadi varga

8. Kaiyadeva Nighantu Mishrakaadi varga

9. Bhavaprakasha Nighantu Hareetakyaadi varga

10. Raja nighantu Pippalyadi varga

11. Shaaligrama nighantu Hareetakyaadi varga

12. Nighantu Adarsha Chitrakaadi varga

13. Mahoushadi Nighantu Mahoushadhi varga

14. Amarakosha Vanaushadhi varga

Table 1.1 Showing Gana And Varga according to different classics

Drug review…


Paryaya Nama: Sr. No

Grantha → Synonyms ↓

Cha. Sa.

Su. Sa.

A. san.

DN21 MPN22 KN23 BPN24 RN25 SGN26 Mah. N.27

1. Agni + + + + + + - + - - 2. Anala - - - + - + + + + + 3. Aruna - - - + + + - + - - 4. Chitrapali - - - - - - - + - - 5. Chitrka + + + + + + + + + + 6. Chitranga - - - - - - - + - - 7. Chitrabanu - - - + - - - - - - 8. Dahana - - - + + + - + - - 9. Daruna - - - + + + - + - - 10. Dvipi - - - + - + - + - - 11. Havi - - - - + - - - - - 12. Hutabhuk - + - - + + - - - - 13. Hutasho - + - - - + - - - - 14. Jwala - - - - - + - - - - 15. Jwalana - - - - - + - - - - 16. Jyothi - - - - - + - - - - 17. Jyotishka - - - + - - - + - - 18. Krishana - - - + - - - + - - 19. Katu - - - + - - - + - - 20. Maali - - - - + - - - - - 21. Pachi - - - - + - - - - - 22. Paalaka - - - - - - - + - - 23. Paali - - - + - + - - - - 24. Paathi - - - + - + + + + + 25. Paavaka - - - + - + - + - - 26. Shabala - - - - - - - + - - 27. Shatha - - - - - + - - - - 28. Shardula - - - - - - - + - - 29. Shikha - - - - - + - - - - 30. Shiki - - - + - - - + - - 31. Shura - - - - - - - + - - 32. Ushana - - - - - - + - + + 33. Vallari - - - + - - - - - - 34. Vanhi - - - + + + - + - - 35. Vanhinama - - - - + - - - - - 36. Vyala - - - + + + + + + +

Table 1.2 showing synonyms of Chitraka

Drug review…


ÌlÉÂÌ£ü 28, 29, 30:

ÍcÉ§ÉMü – ÍcÉ¨ÉÇ oÉÑÎ®Ç §ÉÉrÉiÉå CÌiÉ| (pÉÉ. SÏ)

cÉåiÉÍ¶ÉiÉç, ÍcÉiÉÉå eÉlÉÉlÉç §ÉÉrÉiÉå CÌiÉ| (ÌlÉ. AÉ)

It improves and maintains agni. Therefore, it helps in protection of buddhi (mental

faculty) and proper health.

ÍcÉ§ÉMü – ÍcÉ§ÉçÇurÉÉbÉëÌlÉpÉÉå ÍpÉlÉÌiÉ oÉWÒûzÉÉå aÉÑsqÉÉlÉiÉÍ¶É§ÉMüÈ CÌiÉ | (lÉÉ.Ã.ÌuÉ.)

It hunts immediately many diseases like Gulma etc similar to vyaagra, so called as

Chitraka.

AlÉsÉ – AÎalÉiÉÑsrÉÈ EwhÉ:xmÉzÉåïuÉÏrÉåï cÉ|| (lÉÉ.Ã.ÌuÉ.)

It acts corrosively both internally and externally.

SWûlÉ – SWûiÉÏÌiÉ SWûlÉÈ|

It causes ulceration and burning sensation when applied over the skin.

mÉÏPûÏ – ÌmÉPûÌiÉ ÌWûlÉÎxiÉ xÉqrÉMçü ÌuÉsÉzlÉÉÌiÉ uÉÉ aÉëWûhÉÏ MÑü¸ÉÌS UÉåaÉÉlÉç uÉÉiÉÉÌSSÉåwÉÉÇ¶ÉåÌiÉ| (ÌlÉ.AÉ.)

It completyely cures Grahani, Kushta and subsides aggravated doshas also.

uÉÎlWûxÉÇgÉMü – uÉÎlWûÈ xÉÇgÉÉ rÉxrÉ |

uÉÎlWûmÉrÉÉïrÉlÉÉqÉMüÉ CirÉjÉïÈ| (pÉÉ. SÏ.)

It is known with all the names of fire.

Drug review…


Vernacular names (names in different languages) 31: Arabic Shitaraj, Shitaraz

Bengal Chita, Chitraik, Chittu, Sufaid

Burma KanChopphiju, Kinkhenphiu

Canarese Chitramula, Chitramulike, Mulike,Vahni

Chinese Pai Hua T’enga, Pe Hoa T’en

Deccan Chitarmul, Chtarmulam

English Ceylon Leadwort, White Flowered

Leadwort

Farasi Vekhvaranda,Bekhbarandar,Shitarak

French Dentelaire de Ceylon

Gujarathi Chitro, Chitra, Chitrapitaro

Hindi Chita,Chitra,Chiti,Chitraka Lalchita,Raktachitra,Lalchitarak

Kannada Chitramool, Bilay

Latin Plumbago zeylanica Linn.

Malayalam Tumpukotuveli

Marathi Chitraka, Chitramula

Nepal Chitu

Persian Bighbarindeh, Shitarak, Shitirik

Punjabi Chitraka

Sanskrit Chitraka, Agni, Anala, Dahana, Daaruna, Etc

Simhalee Ellantitul, Sudunitul

Tamil Adigaraddi, Akkini, Angodiveli, Kanilam

Telugu Agnimata, Chitramulamu, Tellachitramulamu

Urdu Chitalakri

Uriya Chitamulo, Chitaparu, Krishanu

Table 1.3 showing different Vernacular names of Chitraka

Drug review…


Types of Chitraka according to various granthas:

Chitraka is one of the important drugs in indigenous medicine and recognized mainly

based on the color of the flower.

According to Acharya Vagbhata 32 - Chitraka is of three kinds i.e. Pita, Sita and Asita.

Pita is yellow flowered, Sita white flowered and asita (Krishna) blue flowered variety. In

conformity with the above statement of Vagbhata, Asita variety is the best variety used as

Rasayana.

According to Rajanighantu 33, it is of two types i.e. Shwetachitraka and Raktachitraka.

Red flowered type is considered more potent with its properties than white coloured and

hence the few synonyms used in this context like, Atidipya, Dipyagni, are in

confirmatory with this statement. The other synonyms of Raktachitraka mentioned as

Kala, Vyala, Kalamoola, Maarjara and Chitranga.

According to Shaligramanighantu 34 it is of three types i.e. Shwetachitraka,

Raktachitraka and Krishnachitraka. The author has described the therapeutic uses of

Rakta Chitraka and Krishna Chitraka in detail.

Drug review…


Rasapanchaka of Chitraka: Sr

no

Grantha Rasa Guna Veerya Vipaka

1. Charaka Samhita 35 Katu Ushna Ushna Katu

2. Dhanvantari nighantu 36 - Ushna Ushna Katu

3. Madanapala nighantu 37 - Laghu, Rookhsa, Ushna Ushna Katu

4. Kaiyadeva nighantu 38 Tikta, Katu Laghu, Rookhsa, Ushna Katu

5. Bhavaprakash nighantu 39 - Laghu, Rookhsa, Ushna Ushna Katu

6. Raja nighantu 40 - Ushna Ushna Katu

7. Shaligrama nighantu 41 - Laghu, Rookhsa, Ushna Ushna Katu

8. Mahoushadha nighantu 42 - Laghu, Rookhsa, Ushna Ushna Katu

Table 1.4 showing rasapanchaka of Chitraka according to different classics

Chitraka is not having prabhava property.

It is evident from the above table that maximum numbers of the authors have accepted

Raspanchak as below:

Rasa : Katu.

Guna : Laghu, Ruksha, Ushna

Veerya: Ushna

Vipaka: Katu

According to Kaiyadeva nighantu, Chitrka is tridoshahara. It acts as Kaphahara due to its

Katu rasa, due to its Tikta rasa it acts as Pittahara and as Vatahara due to its Ushna guna.

Drug review…


Karma according to different classics: Sr. No

Grantha → Karma ↓

Cha.Sa.

Su. Sa.

A. san.

DN43 MP N44

KN45 BP N46

RN47 SG N48

Mah. N.49

1. Vaatahara - - - - + + + + - +

2. Pittahara - - - - - + - - - -

3. Kaphahara - + - + + + + + - +

4. Lekhana + - - - - - - - - -

5. Bhedana + - - - - - - - - -

6. Deepana + + - - - + - - - -

7. Triptigna + - - - - - - - - -

8. Arshoghna + - - - - - - - - -

9. Shoolaprashamana + - - - - - - - - -

10. Paachana + + - - - + + - + +

11. Graahi - - - - + - + - + +

12. Rochana - - - - - + - - - -

13. Rasayana - - + - - - - - - -

14. Kanduhara - - - - - - - + - -

15. Krimihara - - + - + + + + + +

16. Medogna - + - - - + - - - -

17. Vishahara - + - - - - - - - -

18. Vruna shodhaka - + - - - - - - - -

19. Yonidoshahara - + - - - - - - - -

20. Stanyashodhaka - + - - - - - - - -

21. Netrya - + - - - - - - - -

22. Vrushya - + - - - - - - - -

23. Medya - + - - - - - - - -

Table 1.5 showing karmas of Chitraka according to different classics

Drug review…


Rogaghnata according to different authors:

Sr.

No

Grantha →

Rogaghnata

↓

Cha.

Sa.

Su.

Sa.

A.

san.

DN50 MPN51 KN52 BPN53 RN54 SGN55 Mah.

N.56

1. Arsha + + + + - + + + +

2. Atisara + - - - - - - - -

3. Ama - - - - - + - - - -

4. Grahani + - + + + + + + + +

5. Gulma + - - - - - - - - -

6. Shoola + + + - - - - - - -

7. Kandu - - - - - - - + - -

8. Krimi - - + - + + + + + +

9. Kushta + + + - + + + - + +

10. Kasa + - + + - + - + +

11. Kshaya + - - - - - -

12. Meha + + + - - - - - - -

13. Pandu - + + - - - - - -

14. Shwitra - + + - - - - - - -

15. Swarabheda - + - - - - - - - -

16. Shotha + - - + + + + + + +

17. Udara + + - + - + - -

Table 1.6 showing rogaghnata of Chitraka according to different classics

Therapeutic uses of Chitraka 57:

1. In medhoroga, Chitraka root powder should be taken with madhu. (Vangasena 22)

2. Bark of Chitraka is pasted with in a jar, curd or buttermilk prepared in the same, on

intake it destroys piles. (Cha.Chi 14/76, Su.Chi.6/13, A.Hru.Chi. 8/30, VM 5/18)

Drug review…


3. Paste of Chitraka is mixed with Shunti and sourgruel is applied to Arsha.

(Cha.Chi14/68)

4. Powdered Chitraka root bark along with takra cures Atisara. (Cha.Chi.10/119)

5. Chitraka gruta is indicated in Udararoga. (Cha.Chi. 13/116)

6. In Kushta, Chitraka moola is indicated daily, along with gomutra. (Su.Chi. 9/45)

7. In Shwitra, gomutra mixed with Chitraka, Trikatu, madhu should be kept in a jar of

ghee for a fortnight. Than, patient should thereafter take it daily. (Su.Chi. 9/39)

8. In Sikatameha, Chitraka root decoction is indicated. (Su. Chi. 11/8)

9. Chitraka root powder and Bala root powder each one tola along with warm water

should be given in Pandu. (S.U.44/26)

10. Chitraka sidda ghruta is indicated in Sangrahani, Gulma, Shotha, Udararoga and

Pleeha. (C.D.)

11. Chitraka root should be applied in Shlipada with Devdaru.(C.D.)

12. To perforate the abscess, it is applied on wound. (C.D.)

13. Acharya Vagbhata described the details regarding the use of Chitraka root powder as

Rasayana. (A.H.U.39/62-65)

14. By preparing Ghruta with Chitraka mixed curd and again adding Chitraka root

powder and Takra Ghruta will be prepared and can be used in the patient suffering from

Shotha, Arsha, Atisara, Vataj Gulma, Prameha etc.(Ch.Chi.17/55,56)

Part used: Root & Root bark according to all classics.

Dose: ½ to 2 Masha 58

Powder – 1-2gm 59

Decoction – 25-50ml 60

Drug review…


Toxic effect 61: In small doses, it acts as a sudorific and stimulates the contraction of the

muscular tissue of the heart, intestine and uterus. In large doses, it causes death from

respiratory failure. It has toxic effect mainly on lung, liver and uterus. When applied

externally, the roots produce painful irritation and blisters. While administered internally

they act as narcotic irritant poisons, producing pain in the stomach, thirst, vomiting and

diarrhea.

Antidote 62: For lung, mastagi and gum acacia and for liver, rose flower and sandalwood

should be used.

Substitute 63, 64:

In the unavailability of Chitraka, the substitute for it is Danti kshara and Apamarga

mentioned by Bhavaprakasha poorvakhanda in Mishraprakarana.

While Praval and Manjistha mentioned by Unani Dravyagunadarsha.

Adulterant 65: Plumbago indica Linn. (Syn. P.rosae Linn.) commonly known as Rakta

Chitraka is used for the same conditions as P. zeylanica.

Vishistha yogas:

Sl.no

Vishistha yoga Uses

References

1. Hingusaurchalaadya gruta Vataja gulma Cha.chi.5/69

2. Hingvaadi choorna Vatakaphaja gulma Cha. chi. 5/80

3. Bhallatakadhya gruta Kaphaja gulma, Pleeha,

Grahani, Shwasa, Pandu

Cha. chi.5/146

4. Dantihareetaki Gulma, Shootha, Arsha,

Aruchi

Cha. chi.5/155

6. Chitrakadi lepa Shwitra Cha. chi.7/170

7. Mahapanchagavya gruta Apasmara Cha. chi.10/20

8. Chitrakadi gruta Shotha, Arsha, Gulma Cha. chi.12/56

Drug review…


9. Chitrakadi udvartana Shotha Cha. chi. 12/72

10. Pippalyadi choorna Udara roga Cha. chi.13/79

11. Vidangaadikshara Gulma, Pleeha Cha. chi.13/80

12. Panchakola gruta Udara,Shotha,Arsha, Gulma Cha. chi.13/112

13. Kshra vatika Shotha, Jalodara Cha. chi.13/163

14. Pippalyadi dwitiya pralepa Arsha Cha. chi.14/54

15. Chavyadi gruta Arsha Cha.chi. 14/108

16. Dantyarishta Arsha Cha. chi.14/145

17. Chitrakadi gutika Grahani Cha.chi.15/96-98

18. Chitrakadi leha Kasa Cha. chi.18/173

19. Shaddharana yoga Vatavyadhi Su. Chi. 4/4

20. Patralavana vatavyadhi Su. Chi. 4/30

21. Chitrakadi taila Bhagandhara Su. Chi. 8/50

22. Chitraka kwata Sikatameha Su. Chi.11/9

23. Dhanvantara gruta Pramehapidika Su. Chi. 12/5

24. Navayasa loha Prameha, Kushta, Shotha Su. Chi.12/11

25. Shtaphala gruta Udara, gulma, Shotha Su. Chi.14/14

26. Chitraka rasayana Shwitra Su. Chi 28/3

27. Madhukadi gruta Arsha A.Hru. Chi.8/130

28. Soorana modaka Arsha A.Hru. Chi.8/157

29. Chitrakadi kwata Shoola, Anaaha, Vibhanda A.Hru. Chi. 14/48

30. Tryushanadi gruta Vataja gulma A.Hru. Chi. 14/21

31. Chitraka gruta Udara A.Hru. Chi.15/7

32. Chitrakadi kalka Udara A.Hru. Chi. 15/42

33. Rohitaka grita Pleehavruddi A.Hru.Chi15/93

34. Lakshadi choorna Kushta A.Hru. Chi. 19/41

35. Vidangaadi pindi Kushta A.Hru. Chi. 19/45

36. Shashaankalekhadi lepa Kushta A.Hru. Chi. 19/46

37. Shwitranashaka lepa Shwitra A.Hru. Chi. 19/64

38. Gomutrasava Shwitra A.Hru. Chi. 20/7

39. Vyoshadi yoga Stoulya, Hridroga, Kamala A.Hru. So. 14/25

40. Chitraka guda Agnimandya Bhai. Ra. 10/273

Drug review…


Table 1.7 showing vishishta yogas of Chitraka

41. Agnitundi rasa Agnimandya Bhai. Ra. 10/94

42. Agnimukha lavana Agnimandya Bhai.Ra.10/86-88

43. Chitraka haritaki Kshaya,kasa,peenasa, gulma Bhai. Ra.63/28

44. Chitraka taila Nasarsha Bhai. Ra. 63/34

45. Navaka guggulu Medoroga Bhai. Ra. 39/43

Drug review…


Latin name: Plumbago zeylanica Linn.

Plumbum: Lead

Plumbago: That cures lead palsy

Zeylanica: Of ceylon

Taxonomic position of shweta chitraka:

According to Benthem & Hooker (1862-1883)

Kingdom - Plantae

Group - Angiospermae

Sub Group - Dicotyledonae

Division - Gamopetalae

Sub Division - Heteromerae

Family - Plumbaginaceae

Genus - Plumbago

Species - zeylanica

Family Characters 66: Plumbaginaceae

The plants of this family are perennial herbs or shrubs with narrow leaves, without

stipules, and bears water or chalk glands.

Stem - Erect or sometimes climbing.

Leaves -Often radical rosulate.

Inflorescence -Raceme, each flower having two lateral bracteoles, which always remain

Drug review…


sterile is found in Plumbago.

Flowers - Occur in terminal scapes or peduncles in panicles. Flowers bisexual, regular.

Calyx - Generally membranous, persistent, sepals connate, in an inferior, tubular, 5-10

ribbed calyx, often hyaline between the ribs.

Corolla - Petal free, 5, sometimes connate at the base in a short tube to which the

filaments are attached, rarely connate in a linear tube, hypogynous.

Stamens - Opposite the petals, 5 filaments adnate below to the corolla or nearly free,

anthers oblong, dorsified.

Ovary - Superior, unilocular, with a solitary basal anatropous ovule with two

integuments borne at the top of a long filiform funicle with the micropyle pointing

upwards. Styles five, opposite the sepals.

Fruit - Membraneous or coriaceous capsule, dry, dehiscent or indehiscent.

Seeds - Cylindrical, pendulous, albumen floury or absent, embryo straight. Among the

histological characters of prominence, the presences of epidermal glands are common

containing palisade and placed perpendicular to the organ. There are also long stalked

glandular shaggy hairs and simple unicellular hairs. The vessels are with simple

perforations and the wood parenchyma has simple pits. Cork develops superficially in the

cortex with chlorenchyma in groups or in the pericycle. Calcium oxalate present or

absent. The cells of the stem and the root are characterized by many special cells filled

with Plumbagin and these are sometimes differentiated like secretary cells.

Genera - This family contains about 10 genera.

Genus Characters 67: Plumbago

Drug review…


Perennial herbs or under shrubs, sometimes scan dent.

Leaves - Alternate, membranous, entire (in one species absent), amplexicaul and auricled

at the base, or with a petiole which is often dilated and amplexicaul.

Flowers - White rose colored, or blue in terminal spikes, bracts and bracteoles shorter

than the calyx, some times minute.

Calyx - Tubular, 5 toothed, clothed with prominent stipitate glands.

Corolla - Hypocrateriform, tube long, slender, limb spreading. With 5 equal or slightly

unequal entire lobes.

Stamens- Hypogynous, free from corolla, filaments dilated at the base, anthers linear

oblong.

Ovary - Attenuated at the apex into a terminal filiform style which divides above into 5

longitudinally stigmatose branches.

Capsule - Membranous, at length circumcises near the base, the deciduous part often

splitting into 5 valves from the base to apex.

Species - 280

Habitat:

A small genus of herbs, under shrubs or shrubs distributed in the tropics. Three species

are recorded from India of which two are considered medicinally important. A perennial,

sub-scan dent shrub found wild in peninsular India and West Bengal and cultivated in

gardens throughout India. While P. rosea is a native of the Sikkim and Khasia.

Drug review…


Habit 68:

Plumbago zeylanica Linn.

Stem - A perennial herb, subscandent, stems 0.6 to 1.5 M., long, somewhat woody,

spreading, terete, striate and glabrous.

Leaves - Thin 3.8-7.5 to 2.2-3.8 cm. ovate, sub acute, entire, glabrous, reticulatly Veined,

shortly and abruptly attenuated into a short petiole, petiole narrow, amplexicaul at the

base and often dilated into stipule like auricles.

Flowers - spikes, rachis, glandular, striate, bracteoles ovate, acuminate, shorter than the

calyx, glandular or not.

Calyx - 1 to 1.3 cm. long, narrowly tubular, persistent, densely, covered with stalked

glands, teeth small with membranous margins.

Corolla - White, slender, tube 2 to 2.5 cm, long, lobes 8 mm, long, obovate-oblong,

acute, apiculate.

Filaments - As long as the corolla tube, anthers exerted just beyond the throat.

Capsule - Oblong, pointed pericarp thin below, thick and hardened above.

Pharmacognostical Study 69, 70:

Macroscopic study of root:

Roots are 30cm or more in length, 6mm or more in diameter as also as short stout

pieces, including root stocks reddish to deep brown, scars of rootlets present; bark thin

and brown, internal structure striated; Odor, disagreeable; taste acrid.

Microscopic study of root:

Drug review…


Transverse section of root shows that the root is nearly circular in out line and it

shows following characters.

Cark - Outer most tissue of cork consisting of 5-7 rows of cubical to rectangular

dark brown cells.

Cortex - Secondary cortex consists of 2-3 rows of thin-walled, rectangular, light

brown cells. Most of the cortex cells contain starch grains. Secondary cortex followed by

wide zone of cortex, composed of large polygonal to tangentially elongated

parenchymatous cells, varying in size and shape, containing starch grains and some cells

with yellow contents. Fibers scattered singly or in a group of 2-6.

Phloem – It is a narrow zone of polygonal, thin-walled cells, consisting of usual

elements and phloem fibers. Similar to cortical zone, phloem fibers are usually in groups

of 2-5 or more, but occasionally may occur singly. Phloem fibers are lignified with

pointed ends and narrow lumen, similar in shape and size to those of secondary cortex.

Cambium – Indistinct.

Xylem – It is light yellow to whitish in color, vessels radially arranged with pitted

thickenings. Medullary rays – These are straight, 1-6 seriate, and cells radially elongated

and filled with starch grains. Stone cells absent.

Propagation & cultivation 71, 72: Its propagation is by seeds and by cuttings of side shoots. The compost mixture

consisting of equal parts of loam, leaf mould and sand is best suited for its cultivation.

Well-drained sunny situation and mild climate are preferable

Plumbago zeylanica can also be propagated by seeds, rooted shoots from the base

of the plant or by semi-ripe cuttings, treated with a growth hormone. Germination is

Drug review…


almost 100% if both ends of the seed are cut before sowing. Seeds germinate in 21–30

days at 21°C. After 3 months storage, germination decreased to 40%.

In vitro propagation: Plumbago zeylanica can be mass-produced using in vitro

cultivation of nodal explants, axillary buds, leaf or root explants and callus cultures. The

roots of the plants produced this way have a significantly higher content of plumbagin

than control plants, and there is potential for commercial cultivation.

Phytochemistry:

Roots contain plumbagin, droserone, elliptinone, nisoshinanolone,

plumbazeylanone, 3-chloroplumbagin, 3, 3’-biplumbagin, napthoquinone-citranone,

zeylnone and isozeylinone. Root bark contains plumbagin. Aerial parts contain free

amino acids. Leaves and stem contain volatile oil 73.

Two plumbagic acid glucosides, 3'-O-beta glucopyranosyl plumbagic acid

and 3'-O-beta-glucopyranosyl plumbagic acid methylester along with five

naphthoquinones (plumbagin, chitranone, maritinone, elliptinone and isoshinanolone),

and five coumarins (seselin, 5-methoxyseselin, suberosin, xanthyletin and xanthoxyletin)

were isolated from the roots of Plumbago zeylanica. All coumarins were not previously

found in this plant. Cytotoxicity of these compounds to various tumor cells lines was

evaluated, and plumbagin significantly suppressed growth of Raji, Calu-1, HeLa, and

Wish tumor cell lines 74.

Napthalene derivatives – the chief component is plumbagin, together with

3-chloroplumbagin, 3,3”-biplumbagin, 3”,6”-biplumbagin(chitranone), isozeylanicone,

zeylanicone, elliptinone and droserone.

Drug review…


Triterpenes – Lupeol and lupenyl acetate have been isolated from the root.

Amino acids – Aspartic Acid, tryptophan, trysonine, threonine, alanine, histidine,

glycine, methionine and hydroxy proline were isolated from the aerial parts 75.

Plumbagin is a plant-derived naphthoquinone possessing a number of

pharmacological activities. It has been shown to have antimicrobial activity. In animals, it

has antimalarial, anticarcinogenic, cardiotonic, antifertilityaction, and anti-atheroslerosis

effects. Plumbagin is named after the plant genus Plumbago, from which it was originally

isolated.

Plumbagin 76:

IUPAC name: 5-hydroxy-2-methyl-naphthalene-1, 4-dione

Chemical formula: C11H8O3

Molar mass:188.17942 g/mol

Pharmocology:

The root of the plant and its constituents are credited with potential

therapeutic properties including atherogenic, cardio tonic, hepato protective and

neuroprotective properties 77.

The roots of Plumbago zeylanica have shown to possess antipyretic,

Drug review…


appetizer, uterotonic, antibacterial, antifungal, antifertility, anticancer(Plumbagin),

anticoagulant, antitumor, hepatoprotective, cytotoxic, and CNS depressant properties 78.

Traditional uses of Plumbago zeylanica 79:

Africa and Asia: Plumbago zeylanica is very popular as a remedy for skin diseases,

infections and intestinal worms, especially leprosy, scabies, ringworm, dermatitis, acne,

sores, ulcers of the leg, haemorrhoids and hookworm.

West Africa: The root or the leaves crushed with lemon juice are used as a counter-

irritant and vesicant. The pulped roots or aerial parts are inserted into the vagina as an

abortifacient.

Southern Africa: A paste of the root in vinegar, milk and water and even cold infusion

of Chitraka are used to treat influenza and blackwater fever.

East Africa: Pounded roots are applied to swollen legs. A paste of powdered root or the

root sap is used for tattooing by different tribes. The paste or sap causes blisters and the

new skin has a darker color.

Nigeria: The roots pounded with vegetable oil are applied to rheumatic swellings.

Ethiopia: Powdered bark, root or leaves are used to treat gonorrhoea, syphilis,

tuberculosis, rheumatic pain, swellings and wounds.

Zambia: A root decoction with boiled milk is swallowed to treat inflammation in the

mouth, throat and chest.

Zimbabwe: Plumbago zeylanica root cooked with meat in soup is eaten as an

aphrodisiac, and it helps digestion. A root infusion is taken orally to treat shortness of

breath.

Drug review…


Madagascar: The roots are applied as a vesicant, while in Mauritius and Rodrigues a

root decoction is used to treat diarrhoea and dyspepsia.

Physicochemical standards of Plumbago zeylanica 80:

1. Foreign matter - not more than 3 %

2. Total ash - not more than 3 %

3. Acid insoluble ash - not more than 1%

4. Alcohol soluble extractive - not less than 12 %

5. Water soluble extractive - not less than 12 %

Research profile:

Anti-microbial activity:

A chloroform extract of Plumbago zeylanica showed significant activity against

pencillin and non-pencillin resistant strain of Neissaria gonorrhoea. It also showed

Drug review…


antibacterial activities against Bacillus mycoides, B. pumilus, B. subtilis, salmonella

typhi, staphylococcus aureus and others. Eye drops containing 50μg/ml of

Plumbagin demonstrated significant antibacterial, antiviral and anti chlamydial

effects in eye diseases with few side effects. Aqueous hexane and alcoholic extracts

of the plant were found to show intensive antibacterial activity. The alcoholic extract

was the most active and showed no toxicity when assessed using fresh sheep

erythrocytes 81.

Ethanolic extract of Plumbago zeylanica root was investigated for its antimicrobial

activities against 11 human pathogenic bacteria and 6 phytopathogenic fungi using

disc diffusion method and poisoned food technique respectively. The extract

exhibited good antibacterial and antifungal activities against the test organisms.

Among the test bacteria, Vibrio cholerae was found to be the most sensitive to the

extract showing the highest diameter of zone of inhibition and lowest minimum

inhibitory concentration (MIC) value (200 g/ml). The extract was also very effective

against Escherichia coli and Pseudomonas aeruginosa showing MIC value of 250

g/ml 82.(M Shafiqur Rahman and M Nural Anwar)

Anti-Helicobacter pylori activity of Plumbago zeylanica: The results revealed that

Plumbago zeylanica L. had the highest inhibitory effects against H. pylori 83.

Immnomodulatory activity:

The effect of plumbagin was studied on peritoneal macrophages of BABL/c mice,

evaluated by bacterial activity, hydrogen peroxide production and superoxide anion

release. The bactericidal activity in vivo of plumbagin trated mouce macrophages

Drug review…


was estimated using staphylococcus aureus and in low doses of plumbagin caused a

constant increase in bactericidal activity. It was also seen to exert a similar response

on oxygen radical releases showing a correlation between oxygen radical release

and bactericidal activity. Plumbagin appeared to augment macrophase bactericidal

activity at low concentration by potentiating oxygen radical release, where as at

higher concentration it has inhibitory effects 84.

The antiallergic properties of the 70% ethanol extract from Plumbago zeylanica

stems (EPZ) were investigated in the present study. The extract (500, 1000 mg/kg,

p.o.) dose-dependently inhibited systemic anaphylactic shock induced by compound

48/80 in mice, reduced homologous passive cutaneous anaphylaxis and skin

reactions induced by histamine or serotonin in rats, significant differences were

observed at the dose of 1000 mg/kg 85. (Dai Y et.al)

Anti-inflammatory activity:

A phosphate buffered saline extract of the roots of Plumbago zeylanica stabilizes

red blood cells subjected to both heat and hypotonic induced lyses. A biphasic

response and the reduction in the enzymatic activity of alkaline and acid

phosphatases were observed and adenosine triphosphate activity was stimulated in

liver homogenates of formaldehyde-induced arthritic rats 86.

Anti-cancer activity:

The plumbagin has been reported as having anticancer activity against fibro

sarcoma induced by methyle cholanthrene and P388 lymphocytic leucamia, but not

Drug review…


against L1210 lymphoid leukemia in mice. It is thout to be inhibitor of mitosis. It

has been evaluated against Dalton’s ascetic lymphoma where an inhibition of tumor

growth and a significant enhancement of mean survival time were observed for

trated mice when compared to control group. Peritoneal cell counts are also

enhanced. Plumbagin treated group were able to reverse the change in various

hematological parameters which are a consequence of tumor inoculation. Studies

have shown that plumbagin, when administered in the dose of 4mg/kg body weight

caused tumor regression in rats 3-methyl-4dimethyl aminoazobenzene (3MeDAB)-

induced hepatoma. It reduced levels of glycolytic enzymes such as hexokinase,

phosphoglucoisomerase and aldolase levels, which are increased of in hepatoma

bearing rats, and levels of gluconeogenic enzymes such as glucose-6-phosphatase

and fructose-1,6-diphosphatase which are decreased in tumor hosts 87.

Plumbagin administered intramurally and orally at 2mg/kg decreased tumor growth

by 70% and 60% respectively in rats with methylchloranthrene-induced tumor 88.

Anticancer mechanism of plumbagin, a natural compound, on non-small cell lung

cancer cells: Plumbagin exerted anticancer activity on NSCLC cells by modulating

the pro-survival and pro-apoptotic signaling that causes induction of apoptosis 89.

(Gomathinayagam R et.al.)

Hypolipidemic activity:

When administered to hyperlipidaemic rabbits plumbagin reduced serum

cholesterol and LDL cholesterol by 53-86% and 61-91% respectively. It also

Drug review…


lowered the cholesterol/phospholipids ratio and elevated HDL cholesterol

significantly. Furthermore, Plumbagin treatment prevented the accumulation of

cholesterol and triglyceride in the liver and aorta and caused regression of

atheromatous plaques of the thoracic and abdominal aorta. The animal with

plumbagin exerted more fecal cholesterol and phospholipids 90.

Effect of Plumbago zeylanica in hyperlipidaemic rabbits and its modification by

vitamin E: Effect of ethanolic extract (50% v/v) of Plumbago zeylanica (root)

alone and combined with vitamin E (an antioxidant) was studied in experimentally

induced hyperlipidaemic rabbits. There was significant reduction in serum total

cholesterol, LDL cholesterol and triglyceride levels. Marked reduction was

observed with the formulation of P.zeylanica and vitamin E. The total

cholesterol/HDL and LDL/HDL cholesterol ratios were found significantly

decreased (P<0.05). P.zeylanica showed good margin of safety as determined by

acute toxicity studies in albino rats and albino rabbits, as well as by the absence of

adverse effects on haematological and biochemical parameters in albino rabbits

upto 60 days of administration 91. (Alpana Ram)

Anti-oxidant activity:

At a concentration of 1mM plumbagin prevented peroxidation in liver and heart

homogenates. By comparision with menadione (which is having one hydroxyl

group less) it was suggested that plumbagin may prevent NADPH and ascorbate-

induced microsomal lipid peroxidation by forming hydroquinones. These may

trap free radical species involved in catalyzing lipid peroxidation 92.

Antioxidant properties of Plumbago zeylanica aqueos and alcoholic extract of

Drug review…


roots significantly inhibited lipid peroxidation induced by cumene hydroperoxide,

ascorbate-fe(2)+ and peroxynitrite. It contained high amount of polyphenols and

flavonoids 93. (Tilak Jai C et.al)

Anti-fertility activity:

In the rats treatment during the first weeks of pregnancy abolished certain uterine

proteins resulted in both pre implantationary loss and abortion of fetus. The

uterine endopeptidases (cathepsin D. remin, and chymotropsin) were studied

after the root powder has induced and cathepsin D and remin may play a major

role in maintanence of pregnancy and cymotripsin may be involved in post

abortive involution. Plumbagin, at the dose of 1 & 2 mg/kg body weight

prevented implant, induced abortion in albino rats without any tetragenic effects,

and produced a significant inhibitory effect on copper acetate-induced ovulation

in rabbits 94.

Uterine stimulant activity:

The juice extracted from the root was found to have potent activity when treated

on rat uterus in vitro, as well as on isolated human uterus 95.

Anti-stress activity:

Protective effect of Plumbago zeylanica against cyclophosphamide-induced

genotoxicity and oxidative stress in Swiss albino mice: Plumbago zeylanica was

tested for its possible in vivo protective effect against cyclophosphamide-induced

genotoxicity and oxidative stress in Swiss albino mice. Pretreatment with the

alcoholic root extract of Plumbago zeylanica (250 and 500 mg/kg body weight

orally for 5 days) significantly reduced the frequency of micronucleated

Drug review…


polychromatic erythrocytes (MnPCEs), increased the PCE/NCE

(normochromatic erythrocyte) ratio in the bone marrow, and decreased the levels

of lipid peroxidation products with concomitant changes in the status of

antioxidants. Both doses of Plumbago zeylanica were effective in exerting a

protective effect against cyclophosphamide-induced genotoxicity and oxidative

stress 96.

Shlokas:

ÌlÉÂÌ£ü of mÉrÉÉïrÉ:

Drug review…


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Drug review…


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urÉÉsÉÉå WÒûiÉÉzÉÉå WÒûiÉçpÉÑYmÉÉsÉÏ mÉÉPûÏ cÉ mÉÉuÉMüÉÈ |

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zÉÉÍsÉaÉëÉqÉ ÌlÉbÉhOÕû pÉÔwÉhÉ:

Drug review…


ÍcÉ§ÉMüÉåÅlÉsÉlÉÉqÉÉcÉmÉÉPûÏurÉÉsÉxiÉjÉÉåwÉhÉÈ|

aÉÑhÉMüqÉï:

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Drug review…


UÉeÉ ÌlÉbÉûhOÒ:

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Drug review…


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Disease review…


DISEASE REVIEW

Introduction to Medoroga:

The definition of swastya it self says that the person who is having structural and

functional homeostasis of dosha, dhatu, mala, agni, aatma, indriya and mana governs the

normal physiological functions of the human body 97. Disturbance or imbalance in any

one of the above leads to the origin of disease 98. So, Medoroga is the disease caused by

the disturbance in one of the essential seven component of the body i.e. Meda.

Medo Roga may be correlated with hyperlipidaemia and associated disorders on

the basis of clinical signs and complications of the disease.

Basic concept of Meda:

Literally, the word Meda is derived from root “Jhimida Snehana”. This stands for sneha,

fat, oil etc. It means the substance, which has snigdhatva property, is called Meda. There

are many oily substances in the body like Vasa, Majja etc.

Defination of Meda:

In shabdakalpadrum, it is mentioned that Meda is “Mamsa prabhava dhatu

vishesha” and this is the fourth dhatu. The important function of meda dhatu is to

smoothen the body with its snehana property. “Medayati snehayati anen iti medah”.

Synonyms of Meda:

Mamsaj and Mamsatej

Asthi Kruta

Vasa and Vapa

Disease review…


Formation of Meda dhatu 99:

According to Charaka, the Rakta dhatu is combined with tej, apa and is made

solid by the agni. So that it gets converted into mamsa, that again being digested by its

own agni, “medodhatvagni” and stirred up by the agni and getting combined with the

quality of apa and unctuous substances and finally gets converted into the medodhatu.

Bautik composition of Meda dhatu 100:

qÉåSxrÉqoÉÑpÉÑuÉÉæ.. |

Meda dhatu is mainly composed by Jala and Prutvi mahabhoota.

Pramana of Meda Dhatu 101:

The total quantity of meda is two anjali and the vasa is three anjali. Thus, total

meda content of body is enumerated as 5 anjali and total measurable body elements are

counted as 56.5 anjali. From this proportion, it is evident that total meda content of body

is 11 to 12% approximately. Modern physiology also mentioned the same amount of fat.

This quantity may vary from person to person.

Functions of Medadhatu 102, 103:

According to Sushruta, sneha, sweda, dradhatva and asthipushti are the functions

of medadhatu. Again, netra and gatrasnigdhata are the additional functions of meda

mentioned by astang samgraha.

qÉåSÈ xlÉåWûxuÉåSÉæ SèRûiuÉÇ mÉÑÌ¹qÉxjÉÉlÉÉÇ cÉ |

Snehana: Sneha property helps to keep luster of skin, hairs and eyes etc.

Swedas: Sweda is the mala of meda. Thus meda produces sweda and keeps skin moist.

Asthi poshana: Asthi being its next dhatu, the meda nourishes asthidhatu.

Disease review…


Drudatva: This is possible with the help of snayu the upadhatu of meda. Both snayu and

sandhi are directly related to asthi dhatu. Snayu provides support to asthi and sandhi

helps in joint formation.

Meda protects internal organs by covering them all around allowing their free movements

without injury.

Netra and gaatrasnigdhata : These are the symptoms of sthoulya and may arise through

increased snehana function of meda.

Ashryashrayeebhava of Meda 104:

Kapha dosha resides in meda dhatu.

Thus kapha is ashrayee and meda is ashraya.

Medovaha Srotasa:

The internal transport system of the body is represented as Srotamsi. It has been

given a place of fundamental importance in Ayurevda both in health and disease

condition. Dhatus are nourished through their respective srotases and one srotas cannot

provide nourishment to another dhatu. The Meda dhatu gets nutrition from the preceding

dhatu i.e. Mamsa (Poshaka) through its own srotas called Medovaha Srotas.

Moola of Medovaha Srotas :

Charaka 105 - Vrikka and Vapavahana

Sushruta 106 - Vrikka and Kati

Vagbhat 107 - Vrikka and Mamsa

The three Acharyas have considered collectively that Vrikka as one of the moola

of Medovaha Srotas but vapavahana, kati and mamsa are mentioned as second moola

separately.

Disease review…


Vrikka:

Vrikka, one of the kosthanga formed by the sara of rakta and meda dhatu. Charaka has

considered as “Moola” so these structures must be directly related with fat metabolism.

But, there is no such exact evidence in Modern science as well as Ayurevdic Science. If

we take into the consideration of two structures situated above the two kidneys i.e. Supra-

renal glands as vrikka that fulfils the all aspects of fat metabolism.

Vapavahana:

Vapavahan is also a kosthanga and second root of Medovaha Srotas. Chakrapani has

interpreted it as Tailavartika while Dr. Ghanekar has considered it as omentum, where the

maximum Meda is stored.

Kati:

Acharya Sushruta has given anatomical preference than the physiological point of view in

considering kati as moola of medovaha srotas. Kati is the place where the fat

accumulates.

Mamsa:

Vagbhat has considered mamsa as the moola of medovaha srotas. It is not easy to explain

correctly. But we might have considered the Vasa (Mamsagata Sneha) below the skin and

as such the entire skin may be considered as the moola of Medovaha Srotas 108.

Pathophysiology of Medoroga 109:

According to the principles of Ayurveda, rasa is the main factor for providing

nourishment to the body and rest of the dhatus. rasa dhatu is also responsible for staulya

and karshya. Intake of fat and carbohydrate rich diet and lack of physical exercise gives

rise to origin of agnimandya condition results the production of Ama. Ama increases the

Disease review…


meda dhatu and the medodhatu thus produced makes body sthoola.

Etiology of Medo Roga 110, 111:

According to most of the authors unbalanced diet and sedentary habits are the important

causes of Medoroga. As per the description available in the Ayurvedic classics etiological

factors of Medoroga may be classified as follows –

Dietary Factors: These include atisampurna ahara (over eating), adhyashana

(repeated eating), madhura-guru-sheeta dravya ahara, sleshmala-dravya ahara, ati

meda sevana and ati madya sevana etc.

Behavioral Factors: Responsible behavioral factors for the obesity are diwaswapna

(day sleep), achintana (lack of thinking), avyayama (lack of exercise) lack of

meditation and self discipline.

Hereditary Factors: In addition to above factors hereditary factors also play an

important role in development of medoroga.

Inadvertent Therapeutic Application: Injudicious use of some of the therapeutic

measures i.e. Santarpana and Brimhana may also give rise to obesity.

Etiopathogenesis of Medo Roga:

Disease review…


Nidana sevana

Mandaagni and production of ama

Circulating ama

Nourishement of medadhatu

Conversion of madhura anna in to meda and sneha

Meda dhatu increased in erxess due to over nourishement

Srotoavarodha due to excessive accumulation of meda vata increses

agni increses

Medoroga increased appetite

Samprapti ghataka of Medoroga:

On the basis of various references the Samprapti Ghataka of Medoroga are illustrated

below:-

Dosha: Vata-Kapha pradhana tridoshaja

Kapha:Adhika

Vata (vyana & samaana)- Tama

Pitta (Pachaka) – Tama

Dushya: Rasa, Meda, Majja, Shukra, Oja.

Agni: Jatharagni – Teekshna, Dhatvagni - mandya

Disease review…


Ama: Dhatvagnimandyajanya.

Srotasa: - Rasavaha, Medovaha, Mamsavaha, Udakavaha, Swedavaha.

Srotodushti: Sanga

Adhisthana: Medodhara kala, vapavaha

Udbhavasthana: Amashaya

Vyakta sthana: Sphik, stana, udara

Sanchara sthana: Rasayani

Swabhava: Chirakari

Clinical features of Medoroga as mentioned by Charaka,Sushruta and

Madhava112, 113, 114:

Sl no Clinical features C.S. S.S M. N.

1. Chala Spik, Sthana, Udara + - +

2. Ayurhasa + - +

3. Javoparodha + - -

4. Krichravyavayata + + +

5. Dourbalya + - +

6. Dourghandhyata + + +

7. Swedadhikyata + + +

8. Atikshudha + + +

9. Atipipasa + + +

10. Atinidra - + +

11. Krathana - + +

12. Gadgadhatwa - + +

13. Soukumarata - - +

Table 2.1 Clinical features of medoroga according to different authors

Disease review…


Complications Medoroga 115, 116:

Some of the common complications of Medo Roga are Prameha, Prameha, Pidika,

Bhagandara, Pandu, Kamla, Kotha, Granthi, Galganda, Sotha, Mutra Krichchhra,

Vidradhi, Visarpa, Jwara, Atisara, Arsha, Sleepada, Apachi, Madhumeha, Arbuda and

several Vata vikaras.

According to the concepts of Dalhana, the Vata vikara associated with Medoroga

occurs due to deposition of Meda in the Srotasa (Avritta marga). Such a phenomenon of

Avritta marga occurring in the circulatory system may be considered analogous to

atherosclerosis which leads to several cardiovascular and cerebro-vascular diseases (Vata

Vikara).

Management of Medo Roga 117, 118:

Avoidance of causative factors.

Use of drugs which alleviates Vata, Kapha and Meda in the form of food.

Use of lekhana basti.

Use of drugs having rookshana and chhedana qualities such as Shilajatu, Guggul,

gomutra, Triphala, Yavan, Madhu, Rasanjana, Mugda, Koradoshaka, Shyamaka,

Uddalaka, Lauha Bhasma etc and

Change in the life style performance of Prajagarana, Vayama, may cause removal

of Medo Roga.

These acts on the basis of reduction of formation and accumulation of Medo Dhatu.

Disease review…


LIPIDS

Simple lipids Compound lipids Derived lipids

Triglycerides PhospholipidsWaxes

Lecithin

Glycolipids Others

Cephalins

Sphingomyelins

Steroids Fatty acids

Plasmogens

BASIC CONCEPT OF LIPIDS

Lipids are substances, which are actual or potential esters of fatty acids and insoluble in

water but soluble in hot alcohol, ether, benzene, petroleum ether and acetone119.

Classification of lipids 120, 121:

I. Simple lipids: Esters of fatty acids with alcohols.

(a) Triglycerides (Triacylglycerols): These are the esters of fatty acids with

glycerol. Ex: Omental fat, adipose tissue fat, subcutaneous fat in man and

animals, butter fat variable edible oils.

(b) Waxes: These are the esters of fatty acids with alcohol other than glycerol.

In human body commonest waxes are the cholesterol esters. They are most

abundant in the blood, suprarenal glands, the gonads and the sebaceous glands

of the skin.

II. Compound lipids: These are compounds made up of alcohol, fatty acids and some

other substances like phosphoric acids, choline etc.

(a) Phospholipids: Esters containing phosphoric acid and a nitrogenous base

i.e. lecithin, cephalin.

Disease review…


(b) Glycolipids: Esters containing a carbohydrate and a nitrogenous base i.e.

cerebrosides.

(c) Others: It includes other compound lipids like Sulpholipids which are

esters containing sulphuric acid.

III. Derived lipids: They are compounds which are derived from lipids or precursors

of lipids.

(a) Fatty acids: These are the constituents of all classes of lipids. They contain

C, H & O. They are carboxylic acids and can be represented by the

formula CH3 (CH2)nCOOH.

(b) Steroids: These are the derivatives of complex ring system called

“cyclopentanoperhydrophenanthrene” ring system. Cholesterol, ergosterol,

bile acids, sex hormones, adrenal cortical hormones and the D-vitamin are

some of the important sterol derivatives.

Physiological classification of lipids 122:

The lipids of the body are some times divided in to two groups,

1. Element constant

2. Element variable

1. Element constant: Lipids of this group are made up of that fraction of the body lipid

which is required principally for formation of the cell membrane of the animal cell.

This fraction is not sharply altered in amount by starvation or overfeeding.

Phospholipids fall in this category.

2. Element variable: This is that fraction of lipids which are reduced in quantity

during starvation, because they under go catabolism to provide energy. Conversely by

Disease review…


overfeeding, the element variables amount in the body can be increased. Triglycerides

in the depot fat are element variable.

Fat depots 123, 124:

For storing energy our body uses either glycogen or triglycerides. However

our body can store a maximum of about 500gms of glycogen, while there is no ceiling

for how much triglyceride can be stored.

These stored energies can act as fuels which are ultimately used as ATP.

While 500gms of glycogen can supply our energy requirements for only few hours,

the stored fat can look after the needs of the body for weeks or even months together.

About 12% of the total body weight of a man consists of fat. It is stored in the

body in certain sites known as fat depots.

As storage material fat has many advantages,

Per gram triglycerides yields 9kcal of energy where as glucose yields 4kcal.

Fat occupies minimum space.

It is comparatively light weight.

It can be stored in the body as almost 90% pure form.

It regulates body temperature.

It provides mechanical protection against injury.

Composition of Depot fats:

Depot fat is chiefly composed of mixed triglycerides. Trace of lecithin and

cholesterol, as well as a little amount of polyunsaturated fatty acids.

Distribution of fat in body tissue:

(i) Subcutaneous tissue -50% (ii) Peripheral tissue - 15%

(iii) Mesentery - 20% (iv) Omentum - 10%

(v) Intramuscular connective tissue- 05%

Disease review…


Plasma lipids 125:

Although the lipids are present in both body cells and plasma of blood, but the

composition of lipids in plasma and cells widely vary. Since, the composition of

plasma lipids accurately reflects the actual state of lipid metabolism, so the

composition of plasma lipids is generally studied.

Main plasma lipids:

I. Cholesterol and its esters II. Triglycerides

III. Phospholipids IV. Non-esterified fatty acids

Normal serum lipid values:

Lipid Values(in mg/100ml)

Cholesterol 140-220

Triglycerides 50-150

Phospholipids 150-300

Free fatty acids 5-15

Table 2.2 showing normal serum lipid values

I. Cholesterol 126, 127:

The cholesterol means “solid alcohol from bile”. It is so called as it was first

isolated from gall stones.

The Cholesterol is a waxy, fat-like compound that belongs to a class of

molecules called steroids. It has a molecular formula C27H45OH. It possesses

“Cyclopentanoperhydrophenanthrene nucleus”. Cholesterol is made primarily in liver

(about 1,000 milligrams a day), but also by cells lining the small intestine and by

individual cells in the body.

It exist in two forms in our body,

Free cholesterol: Where the –OH group remains free.

Disease review…


Cholesterol ester: Where the –OH group at C3 is esterified with a fatty acid.

Cholesterol is an important component of biomembranes. Cholesterol is

present in plasma either as free form or esterified. Bile has high concentration of

cholesterol and so bile serves as the major excretory route for cholesterol.

Occurrence:

It is widely present in the body tissues; cholesterol is found largest amounts in

normal human adults.

Brain & Nervous Tissue - 2%

In the Liver - 0.3%

Skin - 0.3%

Intestinal mucosa - 0.2%

Certain endocrine glands Viz - adrenal cortex contains -10% or more Corpus

leutiem is also rich in cholesterol. Cholesterol is present in blood and bile usually a

major constituent of Gall Stones.

Sources:

Exogenous: Dietary cholesterol approximately 0.3gm/day. Diet rich in cholesterol are

butter, cream, milk, egg yolk, meat etc.

Endogenous: The cholesterol obtained by endogenous synthesis.

Biosynthesis of Cholesterol:

Average diet supplies about 0.5 gram cholesterol a day. Another 0.5 gram is

synthesized in the body. The liver and the intestine are the principle sources for blood

cholesterol and synthesize about 1.5 gram each day. Other tissues which synthesize

cholesterol are adrenal cortex, gonads, skin, and intestine. Low order of synthesis

occurs in adipose tissue, muscle, aorta and nervous tissues. Brain of the new born

baby can synthesize the cholesterol while adult brain cannot synthesize the

cholesterol.

Disease review…


Cholesterol synthesis occurs in the cytoplasm and microsomes from the two-

carbon acetate group of acetyl-CoA. The process has following steps,

1. Formation of acetyl-CoA: A molecule of acetic acid is activated by combining with

coenzyme A. The reaction requires energy from breakdown of ATP and is catalyzed

by the enzyme acetyl-coA synthetase.

2. Formation of acetoacetyl-CoA: Two molecules of acetyl-coA condense to form an

acetoacetyl-CoA molecule.

3. Formation of HMG-CoA: The acetoacetyl-CoA now condeses with one more

molecule of acetyl-CoA to form beta-hydroxy, beta methyl glutaryl-Coa(HMG-CoA).

The enzyme which mediates this reaction is called HMG-CoA reductase.

4. Formation of Mevalonic acid: HMG-CoA is reduced by an NADPH+ H+

depending reductase to form mevalonic acid

5. Formation of isopentenyl pyrophosphate: Mevalonic acid now becomes isopentenyl

pyrophosphate, IPP. IPP becomes dimethylallyl pyrophosphate, DPP. IPP as well as

DPP are both isoprenoid units, each having 5C structures.

6. Formation of squalene: One IPP and DPP unit unite with each other to form geranyl

pyrophosphate(GPP) unit which is a 10C structure. GPP now combines with another

IPP to form a fernesyl pyrophosphate, FPP. FPP is a 15C structure. Nextly, two FPP

units combine with each other to produce squalene (a 30C structure).

7. Squalene becomes cholesterol: squalene is hydroxylated and cyclized to become

cholesterol.

Disease review…


Showing the Biosynthesis of Cholesterol:

Acetic Acid + Co-A

Acetyl Co-A synthetase + ATP+Mg++

Actyle Co-A (2mol)

Condensing enzyme

Aceto acetyl Co-A

Acetyl Co-A HMG Co-A synthatase

HMG-Co-A

HMG Co-A reductase

Mevalonic acid

ATP

Isopentenyl pyrophosphate (I.P.P.)

2 mol. I.P.P. condense

Geranyl pyrophosphate (G.P.P.)

1 mol. I.P.P. condense with G.P.P.

Farnesyl pyrophosphate (F.P.P.)

2 mol. F.P.P. condense

Squalene

Lanosterol

Demosterol

Cholesterol

Regulation of Cholesterol Synthesis:

1) Cholesterol synthesis is regulated at the HMG – CoA reductase step. During fasting

there is marked decrease in the activity of HMG Co-A reductase which reduces the

synthesis of cholesterol.

2) Cholesterol synthesis is also inhibited by LDL-cholesterol taken up via LDL

receptor.

Disease review…


3) Diurnal variations are also known to occur both in cholesterol synthesis and

reductase activity.

4) Insulin and thyroid hormone increase the reductase activity, whereas glucagons and

corticosteroids decrease the reductase activity.

5) The amount of cholesterol in diet influences in the endogenous synthesis of

cholesterol and when dietary intake of cholesterol is raised the endogenous hepatic

production of cholesterol falls.

6) Intra luminal concentration of bile acids regulates the intestinal synthesis (Dietschy

et al, 1970). While the absorption of biliary cholesterol limit the rate of hepatic

cholesterol synthesis (Grundyet al, 1969).

7) Substitution of poly-unsaturated and mono-unsaturated fatty acids (naturally

occurring oils) for some of the saturated fatty acids in the diet lowers the blood

cholesterol level.

Factors that Influence Cholesterol Level in the Blood:

Dietary Fats - Increased intake of fats in the diet increases the level of cholesterol

by increased synthesis. Greater amount of saturated fatty acids increases

cholesterol level. Substitution in the diet of saturated fatty acids by poly

unsaturated fatty acids has beneficial effect and lowers the cholesterol levels.

Dietary Cholesterol - Increased feeding of cholesterol in diet decreases

endogenous synthesis and reduces cholesterol level.

Dietary Carbohydrates - Increased consumption of carbohydrates increases

cholesterol levels. Consumption excessive amount of sucrose and fructose cause

increase in plasma lipids particularly Triglycerides and Cholesterol. When ratio

between starch: Sucrose is 1:4, an increase in plasma cholesterol is observed.

Calorie Intake - Intake of excess calories increases cholesterol level

Disease review…


Blood Groups - Cholesterol level found to be slightly higher in the persons

belonging to blood group ‘A & ‘AB’.

Heredity - Heredity factors play greatest role in determining individual blood

cholesterol concentrations. Persons, who are prone to become obese, have a high

level of plasma cholesterol

Vit-B-Complex - Nicotinic acid in large doses has cholesterol lowering effect.

Pyridoxine deficiency produces increase in cholesterol level.

Mineral - In vitro acetate to cholesterol conversion in tissue cell culture depressed

by addition of vanadium and iron salts and increased by chromium and manganese

salts. Conversion of mevalonate to cholesterol is inhibited by vanadyl So4.

Physical Exercise - Hard physical exercise brought about lowering in serum

cholesterol level and increased level of HDL Cholesterol.

Dietary Fibres - Increased fibres in the diet caused an increased excretion of

cholesterol and bile acids in feces.

Functions of Cholesterol:

Structural component of cell membrane.

Acts as precursors in biosynthesis of bile acids. Control cell permeability.

Protects the red cells from being easily haemolysed.

Prevent toxins from entering into the cells.

It is also needed for synthesis of Vitamin-D to form cell membrane.

It helps in the synthesis of steroid hormones of sex glands in adrenal cortex and

synthesis of vitamins.

Cholesterol helps in the synthesis of myelin sheath of nerves and acts as insulator

for nerve impulses.

Disease review…


In human being 60-70% cholesterol is transported by LDL, 20-30% by HDL and

5-10% by VLDL.

Degradation of cholesterol:

Majority of cholesterol present in our body are converted in to bile acids (cholic

acid and allied substances) and it enters the bile acid pool. It is eventually

removed by GI tract.

Some cholesterol enters in to composition of bile, enters intestine and eventually

eliminated by GI tract mostly as corposterol and cholesterol.

Some cholesterol is taken up by endocrine glands (like adrenal cortex/gonads) and

is converted into steroidal hormones, eliminated via urine as steroid glucuronoids.

II. Triglycerides 128:

Triglycerides are esters of three fatty acids and glycerol. They are divided in to

two types according to fatty acid contents.

1. Simple - in which all three fatty acids are same.

2. Mixed - in which all three fatty acids are different.

They are transported primarily as chylomicrones and VLDL but in minor amounts

as LDL and HDL also. They are main form of lipid storage in men.

III. Phospholipids 129:

The major types of body phospholipids are lecithins, cephalins and sphigomyelins.

Phospholipids always contain one or more fatty acid molecules and phosphoric acid

radical and they usually contain a nitrogenous base. Although the chemical structure

of phospholipids are some what variant, their physical properties are similar because

they are all lipid soluble, transported in lipoproteins, and used throughout the body for

various structural purposes, such as for use in cell membranes and intracellular

membranes.

Disease review…


Specific uses of phospholipids:

They are an important constituent of lipoprotein in the blood and are essential for

the formation and function of most of these in their absence, serious abnormalities

of transport of cholesterol and other lipids can occur.

Thromboplastin, which is needed to initiate the clotting process, is composed mainly

one of the cephalins.

Large quantities of sphingomyelin are present in the nervous system; this

substance acts as an insulator in the myelin sheath around nerve fibers.

Phospholipids are donors of phosphate radicals when they are needed for different

chemical reactors in the tissues.

Perhaps the most important of all the functions of phospholipids are participation

in the formation of structural elements mainly membranes within the cells thought

body.

IV. Non-esterified fatty acids (Free fatty acids) 130:

These are basic units of fats. Fatty acids are monocarboxylic acid ranging in

chain length from 6 – 24 carbon atoms. In human body free fatty acids are formed

only during metabolism due to hydrolysis of fat. They are very small fraction in

plasma protein.

Fatty acids can be classified as,

1. Saturated fatty acids: They contain no double bond.

Examples: Palmetic acid, Stearic acid.

2. Monounsaturated fatty acids: They contain only one double bond.

Examples: Oleic acid

Disease review…


3. Poly unsaturated fatty acids: They contain 2, 3 and 4 double bonds.

Examples: Linoleic acid, linolenic acid and arachiodonic acids having 2, 3 and 4

bonds respectively.

Plasma lipoproteins 131, 132:

These are the complex formed by the union of plasma lipids and plasma proteins. The

proteins of lipoprotein are called Apolipoproteins.

Lipids are insoluble in plasma but the lipoproteins are soluble in plasma. Thus as

lipoproteins, the lipids can be transported via plasma.

Thus, the two major functions of plasma lipoproteins are,

i. They are the vehicles for lipid transport and

ii. Via lipoproteins, the different lipids are delivered to different tissues.

Classification of lipoproteins:

(a) Chylomicrons

(b) VLDL

(c) LDL

(d) HDL

(a) Chylomicrons:

Chylomicrons are mainly of intestinal origin and their quantity is increased in

plasma following a fatty meal. The plasma becomes opalescent. They are rapidly

taken up from blood by the adipose tissue, heart and skeletal muscle. Lipoprotein

lipase or clearing factor hydrolyzes the lipids of Chylomicrons (and the VLDL) and

helps their passage in to the tissue cells.

Characteristics of Chylomicrons:

They have a lowest density and largest size.

They contain protein 2% and lipid 98%.

Disease review…


In Chylomicrons lipids are mainly triglycerides.

(b) VLDL (Very low density lipoproteins):

The bulk of VLDL is secreted by the liver in a manner similar to Chylomicrons by the

intestines.

Characteristics of VLDL:

They are of very low density, but heavier than Chylomicrons.

They contain 10% protein and 90% lipids.

In VLDL, lipids are mostly triglycerides, but cholesterol and phospholipids are

also present in good quantities.

(c) LDL (Low density lipoproteins):

LDL are a product of degradation of VLDL and Chylomicrons. This fraction is rich in

cholesterol and is taken up by all cells and metabolized.

Characteristics of LDL:

They are of very low density, but heavier than VLDL.

They contain 20% protein and 80% lipids.

In LDL most abundant lipid is cholesterol.

(d) HDL (High density lipoproteins):

HDL are synthesized by and secreted by the intestine as well as liver.

HDL content of plasma decreases if there is an increase in plasma triglycerides.

Characteristics of HDL:

They have a heaviest density.

They contain about 40% protein and about 60% lipids. In HDL, most abundant

lipid is phospholipids but cholesterol is present in good amount.

Disease review…


Characteristics of lipoprotein:

Table 2.3 showing Characteristics of lipoprotein

Fat digestion and absorption 133:

The term fat means lipids i.e., triglycerides, conjugated lipids like

phospholipids, cholesterol. Most of the foods are in the form of triglycerides.

Cholesterol and phospholipids account for only a minor fraction of food.

Composition Chylomicrons VLDL LDL HDL

Protein % 1-2 7-10 18-22 45-55

Lipid % 99 93 80 50

Major lipid Triglyceride Triglyceride Cholesterol Phospholipids

Cholesterol

Diameter(nm) 80-500 30-100 21.5 7.5-10.5

Mg/100ml

plasma

100-250 130-200 210-400 100-150

Function Transport

Exogenous

Triglycerides

Transport

Endogenous

Triglycerides

Transport of

cholesterol and

phospholipids to

peripheral cells

Proposed to

transport

cholesterol from

peripheral cells to

liver.

Disease review…


Digestion and absorption of triglycerides:

Triglycerides

Digestion in oral cavity by lingual lipase less than10%

Emulsification by bile salts, lecithin, monoglycerides & fatty acids

Surface area of triglycerides increased

Action of pancreatic lipase

2 fatty acids + 1 monoglyceride

Dissolves in micelles of bile acid

Soluble in chyme

Comes in contact with brush border of the enterocyte

Fatty acids & monoglycerides diffuse in to enterocyte of cell membrane

leaving micelles behind

Fatty acid with long chain combines Fatty acid with shorter chain

with Fatty acid binding protein

Triglyceride molecule Absorbed in to portal venous

blood route

Enters in blood

Non esterified fatty acids of

plasma

Disease review…


Digestion and absorption of cholesterol 134:

Major sources of cholesterol in the intestine are food and cholesterol of the

bile. While some of such cholesterol is in free form and much of the cholesterol is

ester cholesterol.

Cholesterol ester

Action of cholesterol ester hydrolase

Free cholesterol + fatty acids

Free cholesterol combines with micelles

Enter in to enterocyte

Free cholesterol is esterified with fatty acid

Cholesterol ester

Enter in to lymph

Cholesterol and lipoprotein metabolism 135,136:

Exogenous Pathway:

Exogenous lipid transport begins with intestinal incorporation of dietary

triglycerides and cholesterol into large lipoprotein particles called chylomicrons

(diameter, 80-500nm) which are secreted into the lymph and subsequently enter the

blood stream. When chylomicrons reach the capillaries of adipose tissue and muscle,

they are digested by an enzyme lipoprotein lipase, which is bound to the surface of the

endothelial cells. Lipoprotein lipase hydrolyzes the triglycerides in the core of the

chylomicrons, and the liberated fatty acids cross the endothelium and enter the

underlying adipocytes or muscle cells, they are then either esterfied again to form

triglycerides for storage or oxidized to provide energy.

After most of the triglycerides have been removed in this fashion, the

chylomicron dissociates from the capillary endothelium and enters the circualtion

Disease review…


again. Its size has been reduced and its content of triglycerides diminished, but its

cholesterol esters remain intact. The particle is now designated as a chylomicron

remnant (diameter 30-50nm). When the remnant reaches the liver it is cleared from

the circulation by a receptor that recognizes two of its protein components,

apoproteins E and B-48. The receptor bound remnant is taken into the hepatic cell by

a process termed receptor mediated endocytosis. Within the cell the remnant is

digested in lysosomes, and the cholesterol esters are cleaved to generate free

cholesterol. The free cholesterol has several fats: it can be used for membrane

synthesis, it can be stored by the liver cell as cholesterol esters, it can be excreted into

the bile either as cholesterol or after conversion to bile acids, or it can be used to form

endogenous lipoproteins that are secreted into plasma.

Endogenous Pathway:

Endogenous lipid transport begins when the liver secretes triglycerides and

cholesterol into the plasma in very-low-density lipoproteins (VLDL: diameter, 30-

80nm.). The major stimulus for such secretion is a high-calorie intake (especially a

high - carbohydrate intake), which induces the liver to assemble triglycerides for

export and storage in adipose tissue. The Triglycerides of VLDL are cleaved in

capillaries by the same lipoprotein lipase that digests chylomicrons. Digestion

produces a VLDL remnant that is designated as intermediate-density lipoprotein

(IDL; diameter, 25-35nm.). After release from the endothelium, the IDL particles

have two metabolic fates. Some of the particles are cleared rapidly by the liver, again

by receptor-mediated endocytosis. The receptor that acts on the IDL particle is called

Low Density Lipoprotein (LDL) receptor. It binds lipoproteins that contain

apoprotein E or B-100 and it therefore interacts with both IDL and LDL particles.

Disease review…


About half of the IDL particles are not cleared rapidly by the liver. Rather

they remain in the circulation, where most of the remaining triglycerides are removed,

and the density of the particle increases further, until it becomes LDL (diameter 18 -

28 nm). LDL circulates for a relatively long time in man (half-life of about 1.5days).

The particles are eventually degraded by binding to LDL receptors in liver and certain

extra hepatic tissues. Circulating LDL constitutes the major reservoir of cholesterol

in human plasma, accounting for 60-70% of the total. When liver or extra hepatic

tissues require cholesterol for the synthesis of new membranes, steroid hormones or

bile acids, they synthesize LDL receptors and obtain cholesterol by receptor mediated

endocytosis of LDL. Conversely, when tissues no longer require cholesterol for cell

metabolic purposes, they decrease the synthesis of LDL receptors.

Reverse Cholesterol transport:

As cells of the body die and as cell membranes undergo turnover, free

cholesterol is continually released into the plasma. This cholesterol is immediately

absorbed into high-density lipoproteins (HDL; diameter, 5-12nm.) and in this location

it is esterified with a long - chain fatty acid by an enzyme in plasma, lecithin;

cholesterol acyltransferase (LCAT). The newly formed cholesteryl esters are rapidly

transferred from HDL to VLDL or IDL particles by cholesterol from transfer protein

in plasma. The HDL promote the removal of cholesterol from the peripheral cells and

facilitates its delivery back to the liver is referred to as reverse cholesterol transport.

This transport is facilitates by the synthesis and secretion of apoprotein E by

peripheral tissues.

In addition to degradation by specific receptors, lipoproteins are also disposed

of by less specific pathways, some of which operate in macrophages and other

scavenger cells. When the plasma concentration of a lipoprotein rises, the rate of its

Disease review…


degradation by such pathways increases. This contributes to deposition of cholesterol

in macrophages of arterial walls (producing atheromas) and macrophages of tendons

and skin (producing xanthomas).

Disease review…


Hyperlipidaemic Condition:

Hyperlipidaemia and hyperlipoproteinaemia are synonyms. It is the condition

when the concentration of one or more plasma lipoproteins exceeds the upper limit of

normal level.

Hyperlipidaemia:

The definition of normal limits is inevitably an arbitrary process and values

will vary according to the locality, sex distribution and age of the population studies.

Statistical definitions based on upper 5 or 10% of the distribution of plasma lipid

levels within a population are often used. Hyperlipidaemia is a rise in plasma

cholesterol and triglycerides. Both hyperlipidaemia and hypertriglyceridaemia appears

to be the important risk factor for atherosclerosis.

It is classified as primary and secondary hyperlipoproteinaemia137.

Primary hyperlipoproteinaemia is due to autosomal dominant or recessive genetic

defects or more commonly, to interaction between weaker polygenic influences and

environmental factors such as diet.

Secondary hyperlipoproteinaemia, on the other hand, result from the physiological

derangements which accompany certain disease status like nephritic syndrome,

diabetes or the ingestion of certain hormones, drugs an chemicals including alcohol.

Causes of secondary hyperlipidaemia:

Secondary hypercholesteramia:

Moderately common: Hypothyroidism

Cholestatic liver diseases

Pregnency

Drugs (diuretcs, steroids, androgens)

Disease review…


Less common: Nephrotic syndrome

Anorexia nervosa

Hyperparathyroidism

Secondary triglyceridemia:

Common: Diabetes mellitus Chronic renal disease

Abdominal obesity Drugs (β blockers, corticosteroids)

Excess alcohol

Hyperlipoproteinaemia 138:

Fredrickson et al, (1967) proposed five types based on change in plasma lipoproteins.

These are enlisted in the tabular format.

Table 2.4 showing Fredrickson’s classification of hyperlipoproteinemias

Of the above hyperlipoproteinemias, type II is most common. Type IV is also fairly

common. Type I, III, and V are rare

Type

Lipoprotein

abnormality

Plasma levels of

Cholesterol Triglycerides

Associated factors

I Chyclomicrons increased

Increased Increased Occurrence rare. Lipoprotein lipase is deficient.

II LDL Increased Increased Increased or normal

Occurrence common. Associated with xanthomata and ischemic heart disease.

III LDL and HDL Increased

Increased Increased Rare occurrence. Xanthomata present.

IV VLDL increased

Increased or Increased normal

Excessive synthesis of lipid from carbohydrate. Occurrence common.

V VLDL & chyclomicrons increased

Increased Increased Uncommon occurrence. Associated with ketotic diabetes.

Disease review…


Atherosclerosis 139, 140, 141:

Atherosclerosis is defined by WHO as variable combination of focal

accumulation of lipids, complex carbohydrates, blood and constituents, fibrous tissue

and calcium deposits combined with its changes of the media. Atherosclerosis is thus

a patchy, nodular type of arteriosclerosis.

Atherosclerosis may protrude into and obstruct vascular lumina, weakens the

underlying media and may undergo serious complications.

Atherosclerosis overwhelmingly contributes to more mortality, approximately

half of all deaths and serious morbidity in the western world than any other disorder.

Coronary artery disease is an important manifestation of atherosclerosis and

myocardial infarction alone is responsible for 20% to 25% of all deaths in the United

States.

Classification:

The lesion of an Atherosclerosis is commonly classified as

Fatty streaks: form the earliest lesions of atherosclerosis. They may be reversible

and appear early in life, particularly in the aorta. They are characterized by

accumulation of lipid-filled smooth muscle cells, macrophages and fibrous tissues in

focal areas of the intima.

Fibrous plaques: These are elevated areas of intimal thickening and represent the

characteristic lesion of atherosclerosis. They appear first in the abdominal aorta,

coronary and carotid arteries. They consist of a central core of extra cellular lipid and

necrotic cells, macrophages and collagen.

Complicated lesions: These are classified fibrous plaques with various degrees of

necrosis, thrombosis and ulceration. These lesions commonly produce symptoms of

ischemia.

Disease review…


Risk factor for atherosclerosis:

Major risk factor:

(a) Non modifiable (b) Potentially controlable

Increasing age Hyperlipidaemia

Male gender Hypertension

Family history Cigarette smoking

Genetic abnormalities Diabetes

Minor risk factor:

Obesity

Physical inactivity

Stressful life

Hormones (Estrogen deficiency, oral contraceptive pills)

High carbohydrate intake

Infection (C. Pneumoniae, Herpes virus, CMV)

Materials and methods…


MATERIALS AND METHODS

The study was designed under the following heading,

1) Preparation of the drug.

2) Physicochemical and Preliminary phytochemical analysis of Chitraka.

3) Experimental study.

1) Preparation of the drug

a) Source of drug:

The genuine quality roots of Chitraka (Plumbago zeylanica) were purchased from

Kajarekar pharmacy, Belgaum. Botanist and other experts verified the root and its

identification were confirmed.

b) Purity, Identity and Strength:

For knowing the Purity, identity, strength and genuinity of the crude drug, it was

subjected to physicochemical tests according to the API (Ayurvedic Pharmacopeia of

India) standards and was confirmed.

c) Drying and Powdering :

The work was carried at Pharmacy of Shri D. G. M Ayurvedic Medical College, Gadag.

i) The drug was subjected to powdering using pulverizer and 20 number sieves were used

to get coarse powder of Chitraka. Then the powder was stored in air tight container.

ii) Fine powder of Chitraka was prepared using 120 number sieves and was stored in

airtight container.

d) Preparation of Extracts:

Alcoholic extraction procedures of Chitraka were carried out in the PG dept of

Dravyaguna, Shri D. G. M Ayurvedic Medical College, Gadag.



Alcohol extract:

Hot continuous extraction method was followed using soxhlet apparatus to get the

alcohol extract of Chitraka. Then the powdered drug held in porus bag or a “thimble”

made up of strong filter paper is placed in the sample chamber of the soxhlet. The

suitable solvent is taken in a round bottom flask and the apparatus is assembled. When

the mixture of the drug and the solvent is heated in a heating mantle, its vapours get

condensed in the condenser and drip on the thimble containing the crude drug, extracting

it by contact. When the level of the liquid in the sample chamber rises to the top of the

siphon tube, the liquid siphons into the flask, this process is continuous and is done until

drug is exhausted. Then the extract is collected and solvent is removed under water bath.

The extract thus obtained was stored in the glass bottle, sealed and kept in refrigerator.

2) Physicochemical analysis of Chitraka 142:

a) Determination of Foreign matter:

Materials: Sample & physical balancer.

Procedure:

100-500 g. of drug sample to be examined was spread in a thin layer.

The foreign matter was detected by inspection with the unaided eye or the use of lens.

Foreign matter was separated and weighed.

Percentage of foreign matter present in air dried drug was calculated.

b) Determination of Total ash:

Materials: Silica crucible, physical balance, desiccators, electric bunsen burner & air

dried drug.



Method:

The clean and dry crucible was weighed. Accurately weighed 2 gms of drug was

taken and placed in this crucible and this was kept in electric bunsen burner.

Temperature was gradually increased up to 500º C until white colored ash was

obtained, including the absence of carbon, cooled in desiccators and weighed.

If carbon free ash is not obtained in this manner, then the crucible was allowed to cool

and the residue was moistened with about 2ml of water or a saturated solution of

Ammonium nitrate R. Dried on water bath, then on a hot plate and ignited to constant

weight. Residue was allowed to cool in suitable desiccators for 30 minutes and then

weighed without delay.The content of total ash in mg per gm of air-dried material was

calculated.

c) Determination of Acid insoluble ash:

Materials: Physical balance, crucible, electric bunsen burner, desiccators, air dried drug

and ash less filter paper.

Method:

To the crucible containing the total ash, 25 ml of diluted Hydrochloric acid was added

and covered with a watch glass and boiled gently for 5 minutes. The watch glass was

rinsed with 5 ml of hot water and this liquid was added to the crucible and filtered. The

insoluble matter on an ash less filter paper was collected and washed with hot water until

the filtrate was neutral.

The filter paper containing the insoluble matter was transferred to the original crucible

and dried on a hot plate and subjected to constant heat.



The residue was allowed to cool in suitable desiccators for 30 minutes and then

weighed again.

The content of acid insoluble ash in mg per gram of air-dried material was calculated.

d) Determination of Alcohol soluble extractive:

Materials: Physical balance, powdered air dried drug, glass stopper conical flask, ethyl

alcohol, vacuum filter, hot plate, water bath, beaker and desiccators.

Method:

Accurately weighed 4gm of coarsely powdered air dried drug was placed in a glass

stopper conical flask.Macerated with 100ml of ethanol for 6 hours shaking frequently

.Then allowed to stand for 18 hours.

Filtered rapidly taking care not to lose any solvent.

25ml of the filtrate was taken in a tarred flat-bottomed dish and evaporated to dryness

on a water bath.

Dried at 105oC for 6 hours and cooled in a desiccators for 30 minutes and weighed

without delay. The content of alcohol extractable matter in mg/g of air dried drug was

calculated.

e) Determination of Water- soluble extractive:

Materials: Powdered air-dried drug, physical balance, glass stopper, conical flask, water,

reflux condenser, filter paper, water bath, beaker and desiccators.

Method:

Accurately weighed 5gms of coarsely powdered air- dried material was placed in a

glass stopper conical flask.



This was macerated with 100 ml of water and weighed to obtain the total weight

including the flask.

The flask was shaken well and allowed to stand for 24 hours.

The flask was attached to a reflux condenser and boiled gently for one hour, cooled

and weighed and readjusted to the original weight by adding water. This was filtered

rapidly through a dry filter.

25 ml of the filtrate was transferred to a tarred flat bottomed dish and evaporated to

dry on a water bath.

This was dried at 105oC and cooled in desiccators for 30 minutes and weighed without

delay. The content of water extractable matter in mg / gm of air-dried material were

calculated.

Preliminary Phytochemical investigations of Chitraka:

Qualitative chemical tests were conducted for aqueous, alcoholic and chloroform

extracts of Chitraka (Plumbago zeylanica) to identify the various Phyto constituents. The

various tests and reagent used are given below and observations are recorded.

Place of work: Preliminary phytochemical investigations of Chitraka were carried out at

at Biogenics, Research and Training Center in Biotechnology, Hubli.

Material:

Drug: Aqueous, Alcoholic & Chloroform extractive sample of Chitraka (Plumbago

zeylanica)

Equipments: Test tube, holder, stand, spirit lamp, pipette, glass rods, beaker 50 ml to

250 ml, conical flask, water bath.



Methods:

1) Test for carbohydrates:

Benedict’s test: Test solution when treated with Benedict’s regent and boiled on

water bath if it shows reddish brown precipitate.

Molisch test: To the 2ml of sample, 2 drops of Molisch reagent is added and mixed

carefully, rundown the concentrated H2SO4 along the walls of tubes carefully. The

purple violet color at the junction of two layers is observed.

Barfoed’s test: Test solution treated with Barfoed’s reagent on boiling water bath

shows brick red precipitate.

2) Test for Alkaloids:

Mayer’s test: Test solution treated with Mayer’s reagent (Potassium mercuric

iodide) gives cream precipitate.

Wagner’s test: Test solution treated with Wagner’s reagent (Iodine in potassium

iodide) gives brown precipitate.

Dragendroff’s test: The filtrate when added with few drops of Dragendroff’s

reagent gives orange red color.

3) Test for Proteins:

Million’s test: Sample solution is added with million’s reagent and heated on a

water bath; protein is stained yellow on warming.

Ninhydrin test: To 1ml of test solution add 5drops of Ninhydrin solution and boil

for 2 minutes.Voilet or purple colored solution indicates the presence of amino

acids and proteins.



4) Test for tannin:

Ferric chloride test: Test solution treated with few drops of ferric chloride

solution gives dark color.

5) Test for Glycosides

Conc. H2SO4 test: 1ml of conc. H2SO4 solution was added to the 1ml of solution

and was allowed to stand for 2 minutes. Formation of reddish color indicates

presence of glycosides.

6) Test for Flavonoids:

Alkaline reagent test: Test solution when treated with sodium hydroxyl solution

shows increase in the intensity of yellow color which becomes colorless on addition

of few drops of dilute acid.

Lead acetate solution: Test solution with few drops of lead acetate solution

(10%) gives yellow precipitate.

7) Test for saponins:

Foam test: Sample solution mixed with saponins and shaken, if there is

formulation of stable forth for one minute it indicates the presence of saponins.

8) Test for sterols:

Salkowaski test: A few drops of concentrated sulphuric acid was added to the 5

ml of sample solution (extract) shaken and allowed to stand and observed the lower

layer. If it turns to red indicates the presence of sterols.

Liebermann Burchard test: The test solution treated with few drops of acetic

anhydride and mixed well. When conc. Sulphuric acid is added from the sides of

the test tube, it shows a brown ring at the junction of the two layers and upper layer

turns green.



Identification by T.L.C

Drug: Extraction of sample (Aq, Alc & pet. ether) which is treated with 1:10ml solute;

solvent like ethyl alcohol with dilution method.

Equipment: Silica gel, TLC kit, hot air oven, standard glass, wattaman glass plate,

beakers, sprayer.

Chemicals: Dragendroff’s reagent, Silica gel, ethyl alcohol.

Method: T.L.C. of the ethyl alcohol extract, aqueous extract, petroleum ether extract of

the sample was carried out as follows.

The silica gel powder mixed with water and made thin slurry, and then with the

help of glass slide, the silica gel was spread on glass plates uniformly. After some times

the air dried plate were kept in a hot oven at 110-1200 C. The samples were loaded on

one end of the plate with the help of capillary tubes, leaving 5 cm from the edge. The

spots were carefully done without allowing them to spread. The spots were air dried and

the spotted plate was gently immersed in presaturated closed, TLC chamber for

development. The development was stopped when solvent front reached to 3/4th of the

plate. The plate was then removed from TLC chamber and the solvent front was

immediately marked with a pencil line. Then the plate was air dried and observed under

UV transilluminator to note the fluorescing spots. Then Dragendroff’s solution is sprayed

on the plates.

Rf value of the spots were found out by using the formula,

Rf = Distance traveled by the solute

Distance traveled by the solvent



3) Experimental study

Place of work:

The study was conducted in PG cum Research center Shri D. G. M Ayurvedic

Medical College, Gadag

Source of animals:

The required number of Healthy albino rats of either sex were selected for

experimental study and maintained in the animal house. In PG cum Research center Shri

D. G. M Ayurvedic Medical College, Gadag.

Examination of the animals prior to the experiment:

All the Wister albino rats were subjected to general check up for sex and weight.

The animals with abnormal behavior and ill health were excluded.

Preparation of animals:

The animals were randomly selected, marked with picric acid to permit individual

identification and kept in their cages for one week prior to dosing to allow for

acclimation to the lab condition.

Data collected prior to experiment:

Data were collected prior to the experiment regarding:

Toxicity study

Aboutfixation of the therapeutic dose

Toxicity study:

LD50 of the alcoholic extract of seeds was more than 1000mg/kg ip in albino rats.

(Sharma et al 1978)

50% ethanol extract of roots showed hypothermic and antagonism to



amphetamine hyperactivity in mice. The LD50 of the extract in the albino mice was

500mg/kg ip. (Bhakuni et al 1969)

Plumbagin administered intramurally and orally at 2mg/kg decreased tumor

growth by 70% and 60% respectively in rats with methylcholanthrene induced tumors. Its

ED50 was 0.75mg/kg. plumbagin was active against p388 lympholytic leukaemia at

4mg/kg and showed antibacterial and antifungal activity against a wide variety of bacteria

and fungi. (I. J. exp. Boil. 1980, 18, 876)

Dose fixation in rat:

Dose was calculated individually based on body weight of the rat. The 1/10th of

the LD 50 of alcoholic extracts of Chitraka considered as the therapeutic dose of the

experiment. The suitable dose for rat was calculated by referring the table of Paget and

Barnes 143.

The antiallergic properties of the 70% ethanol extract from Plumbago zeylanica

stems (EPZ) were investigated. The extract (500, 1000 mg/kg, p.o.) dose-dependently

inhibited systemic anaphylactic shock induced by compound 48/80 in mice, reduced

homologous passive cutaneous anaphylaxis and skin reactions induced by histamine or

serotonin in rats, significant differences were observed at the dose of 1000 mg/kg.

Central nervous system stimulatory action from the root extract of Plumbago

zeylanica in rat: The effects of a 50% ethanol extract of the root of Plumbago zeylanica

(P. zeylanica) were investigated on locomotor behaviour and central dopaminergic

activity in rats. The effects on the ambulatory behaviour were assessed along with the

levels of dopamine (DA) and its metabolite homovanillic acid (HVA) in the striatum after

a single oral dose (100, 200 and 300 mg/kg body weight) of the extract. The extract



significantly increased the spontaneous motility in animals. The ambulatory and rotatory

behaviour in the treated groups were higher than in the control group (p < 0.05). There

were marked differences in the ambulatory behaviour between 100 and 300 mg/kg,

indicating that the responses were stimulatory and dose-dependent. The stereotypic

behaviour which is characteristic of a dopamine agonist showed biphasic effects.

However, there was no significant difference between the groups (p > 0.05). The results

showed that the extract of the root of P. zeylanica specifically enhanced the spontaneous

ambulatory activity without inducing stereotypic behaviour. The neurochemical

estimations revealed elevated levels of DA and HVA in striatum compared with the

control rats (p < 0.01). The levels were higher for the 100 mg/kg treated group than the

other groups. The levels declined by increasing the dosage of the extract to 200 mg/kg

and 300 mg/kg, however, these levels remained higher than the control group. The

relationship between motor activity and levels of dopamine are not parallel. These

behavioural and biochemical results indicated stimulatory properties of the extract of the

root of P. zeylanica, which may be mediated by dopaminergic mechanisms in the rat

brain. (C. P. Bopaiah, N. Pradhan, Phytotherapy research volume 15, Issue 2, pages 153-

156)

Pilot Study:

A pilot study was conducted to determine the therapeutic dose of alcoholic extract

of Chitraka as there were no model experimental studies and standards or prior literature

was available for the study.



Acute toxicity study for alcoholic extract:

In the first schedule the alcoholic extract of Chitraka was administered to a group

of 2 albino rat at the dose of 500mg/kg body weight orally and this dose not caused death

of any animal. Then the dose was gradually increased up to 2000mg/kg and 5000mg/kg

body weight. Even at this dose also death of animal was not noticed. According to OECD

guild lines 420, 1/10 of this dose was considered as safe dose for albino rat.

Calculation of dose:

Standard drug:

Atorvastatin

Dose: 5.5 mg/ kg ip

Test drugs:

i) Alcohol extract:

Dose: 200mg/kg/day/p.o

ii) Chitraka churna:

Human dose for therapeutic use according to API is 1-2gm.

On conversion to rat dose referring the table of Paget and Barnes.

Rat dose = Human dose X 0.018

= 2000mg X 0.018

= 36mg/200gm or 180mg/kg

Mode of Administration:

The test drugs in a suspension formed in water and vehicle to control were

administered according to the body weight of the animals by oral route with the help of

no.3 gastric catheter sleeved onto a syringe. The test drugs (Alcohol extract and churna of



Chitraka), standard drug (Atorvastatin) was administered once daily. The control group

rats were fed with plain distilled water

Vehicle for the administration of drug:

Alcoholic extracts and Chitraka churna were administered by making the

suspensions with distilled water.

Feeding schedule:

Quantity of food suggested for rats’ weighing about 150 – 200 grams is about

15 – 20grams/day was provided. Ready made feed prepared by Gold Mohur rat

laboratory animal, Gold Mohur food and feeds ltd. Pirojshahnagar, eastern express

highway, vikhroke east, Mumbai 400079, sold by “Shri Venkateshwara enterprises, No

4303, 13th main, 2nd cross, subrahmanya nagar, Bangalore-21 was procured and used.

Maintenance:

All the animals were maintained at animal house of Shri D. G. M Ayurvedic

Medical College, Gadag, under identical conditions of place, light, temperature, food and

other conditions. All the cages were used to be washed with detergent followed by

disinfectant phenol solution to maintain the hygiene. After cleaning the cages, the

bedding material was prepared using paddy husk and it was changed daily

Experimental protocol:

To study the hypolipidemic effect of Chitraka on albino rats of either sex,

glucocorticoid induced hyperlipidaemia model was selected,

Procedure:

Hydrocortisone sodium succinate (10mg/kg ip) was administered for 2 weeks to 4

group of animals i.e., for group 2 – 5, for induction of hyperlipidaemia. One group of



animal was administered saline and served as normal. After 2 weeks the animals in

different groups i.e., group 3 -6 received treatment for 4 weeks.

After 4 weeks of treatment, the blood was drawn; serum was separated and

analyzed for blood glucose and blood lipid levels. The samples of liver and aorta tissues

were excised out immediately after sacrifice, cleaned of extraneous tissue, cut into pieces

of 3-5 mm thickness and transferred to 10% formalin solution. The samples were sent for

histo-pathological study.

Protocol of experimental study:

Sample: 36 albino rats of either sex are selected randomly and grouped in to 6 groups

consisting of 6 animals in each group.

Inclusive criteria: Healthy albino rats weight – 180 – 230gms.

Exclusive criteria: Other wise does not full fill above condition.

Sl. No Group Study

1. Normal control Vehicle only

2. Hyperlipidemic control Hydrocortisone sodium succinate (10mg/kg/day i.p)

3. Trial group - A Alcoholic extract of Chitraka (200mg/kg/daily, p.o)

4. Trial group - B Churna of Chitraka (180mg/kg/daily, p.o)

5. Standard group Atorvastatin (5.5mg/kg/day, i.p)

6. Trial group - C Chitraka churna to normolipid rats (180mg/kg/daily, p.o)

Table 3.1 showing the protocol of experiment

Study duration: 6 weeks

Statistical analysis: The data collected were statistically analyzed by using ANOVA

followed by Tokey-Kramer multiple comparison test with the consultation of

biostatistician.

Observations & Results…


OBSERVATIONS AND RESULTS

In this section the observations and results are recorded under following headings,

Results of physicochemical analysis.

Observations made during the preparation of the drug.

Results of phytochemical analysis.

Observations and results of Thin layer chromatography (TLC).

Observations and results of pilot study.

Statistical and schematic analysis of the data pertaining to the experiment in

respect of normal control, hyperlipidaemic control, standard drug treated and test drug

treated groups.

Comparison of results within each group and in between the groups.

Results of physicochemical analysis:

The prepared coarse powder of Chitraka (Plumbago zeylanica) was undertaken

for physicochemical analysis and the following results were noted.

Sl.

no.

Test Values %

w/w

Standard values

(API)

1 Foreign matter 1.26% Not more than 3%

2 Total ash 2.65% Not more than 3%

3 Acid –insoluble ash 0.55% Not more than1%

4 Water soluble extractive 16% Not less than 12%

5 Alcohol soluble extractive 15% Not less than 12%

Table 4.1 showing the Physico chemical values of Chitraka

Result of analysis: The sample is confirmed to API standards with respect to above tests

and hence the sample can be declared as of ‘Standard quality’.



Observations regarding preparation of drug:

Preparation of Chitraka churna:

The dried, cleaned roots of Chitraka weighing 4 kgs was procured, then 4 kgs of

drug was subjected to coarse powdering under 20 number mesh and 4 kgs of dry drug

yielded 3.75kgs of coarse powder.

The other 500 gms of drug was subjected to fine powdering under 120 number

mesh and yield was 300gms of fine powder.

1 kgs of course powder was used to prepare the alcohol extract and remaining

kept unused in airtight container.

Observations during preparation of alcohol extract:

By appropriate technique the coarse powder of Chitraka was filled in the round

fold of filter paper i.e. in thimble in sauxhlet apparatus. So that it cannot obstruct any

path ways of sauxhlet apparatus and uniform temperature is maintained.

During each batch, the cycles were continued up to extractive factors of the

powder were get completely extracted in to the solvent, then and then only every batch

was stopped. It was observed that it took around 30 cycles for complete extraction.

After extraction solvents were distilled off.

Liquid extraction taken off was concentrated on hot water bath until it became

semisolid.

1 kg coarse powder of Chitraka yielded 140 gms of (14%) alcohol extract, which

was thick in consistency, dark brownish colored with characteristic smell and pungent

taste. When alcohol extract was mixed with water the color of the mixture was brownish



in appearance.

Observations of prepared Chitraka churna:

The fine powder of Chitraka prepared using 120 number mesh was brown in color

with pungent taste and irritant odor.

Results of phytochemical analysis:

Sl. No.

Tests Aqueous ext.

Alcoholic ext.

Chloroform ext.

1. Test for carbohydrates

a) Molisch’s test

b) Benedicts test

c) Bradford’s test

+

+

+

+

+

+

+

+

-

2. Test for proteins

a) Ninhydrin test

b) Millon’s test

-

+

-

+

-

+

3. Test for alkaloids

a) Mayer’s test

b) Dragendroff’s test

c) Wagner’s test

+

-

-

+

+

+

-

+

-

4. Test for glycosides

a) Conc. Sulphuric acid test

+

+

+

5. Test for tannin

a) Ferric-chloride test

+

+

-

6. Test for flavonoids

a) Alkaline magnet test

b) Lead acetate solution test

+

+

-

+

-

+

7. Test for saponin

a) Foam test

+

-

-

8. Test for steroids

a) Salkowaski test

b) Libermann Burchardt test

-

-

+

+

+

+



Table 4.2 showing phytochemical analysis of Chitraka

Observations of Thin layer chromatography (TLC):

One gram of the Chitraka sample was refluxed with water, alcohol and petroleum

ether (20ml) for an hour and filtered. The extracts were used for the analyses.

The Silica gel slurry was spread on glass plates uniformly with the help of glass

slide.

The samples were spotted with the help of capillary tubes carefully, without allowing

spreading. A space of 2cm was maintained between each spot.

The chromatogram developed by the ascending technique. Development was

allowed to proceed until the solvent front has traveled the 3/4th distance.

First, plate was observed under UV transilluminator to note the fluorescent spots.

Then Dragendroff’s solution is sprayed on the plates.

The distance traveled by the solvent front was noted to be12.2cm. Rf value of the

spots were then found out by using the formula

Rf = Distance traveled by the Solute

Distance traveled by the solvent



Results of TLC:

Stationary phase: Silica Gel G

Mobile Phase: Butanol: Acetic acid: water (4:1:5).

Detection: 312 nm and Drangendroff’s reagent.

Table 4.3 Results of TLC

Sl.

No

Plumbago

zeylanica Linn

Sample+solvent

TLC

plate

system

Detector Rf

Values

Spot

colour

Result

1

2

3

4

5

6

Water extract

Alcohol Extract

Petroleum ether

extract

Water extract

Alcohol Extract

Petroleum ether

extract

Silicagel

G

Silicagel

G

Silicagel

G

Silicagel

G

Silicagel

G

Silicagel

G

Ultra violet

(312 nm)

Drangendroff’s

reagent

0.188,

0.655,

0.696

0.662

No bands

0.655

0.696

0.672

Fluoresce

nt green

Fluoresce

nt green

--

Orange

Orange

Orange

Present

Present

Absent

Present

Present

Present



PLATE –4 @ 312 nm

@ Drangendroff’s reagent



Observations and results of the Pilot study:

Acute toxicity study of alcohol extract of Chitraka:

In the first schedule, groups consisting of 2 albino rats in each, received drug at

the dose of 500 mg and 1000 mg/kg body weight orally in single dose and no death was

seen during observation (even after 12 days).

In the second schedule groups consisting of 2 albino rats in each received drug at

the dose of 2000 mg and 3000 mg/kg body weight orally in single dose, did not show any

death during observation time period (even after 12 days).

Third schedule consisted 5000mg/kg body weight given orally and it also did not

cause any death of animals in that group.

Though 5000mg/kg body weight given orally did not cause any death of animals,

still we decided to consider the 1/10 of 2000 mg as the safe dose for albino rat according

to OECD guild lines 420.



Results of the experiment:

Master Chart

Groups SN

Mark Lipid levels(Mg/dl) TC TG HDL-C LDL-C VLDL-C

Serum glucose (Mg/dl)

1 Head 89.5 120 40.5 22 24 62.8 2 Body 96.3 115 42.8 30.5 23 65.1 3 Tail 87.1 106.8 39.3 26.44 21.36 59 4 Rt ft lb 90.5 110 41.2 27.3 22 64 5 Rt hd lb 106 125 36.7 44.3 25 56

1.Normal control (G1)

6 Lt hd lb 79 104.7 37.2 21 22.8 66.5 1 Head 140.5 155.3 31.5 77.9 31.06 79.6 2 Body 138.3 148 31.8 76.9 29.6 81.2 3 Tail 122.7 130 33.4 63.3 26 78.5 4 Rt ft lb 143.3 160.5 30.8 80.4 32.1 77.9 5 Rt hd lb 130 143.3 29.5 71.84 28.66 88

2.Hyperlipi

demic control (G2)

6 Lt hd lb 151.7 183.3 32.4 82.64 36.66 85.5 1 Head 108.4 123.8 38.4 57.2 27.2 67.5 2 Body 118.7 114.7 36.6 57.8 24.2 70.3 3 Tail 109.2 124.5 33.35 50.95 24.9 69 4 Rt ft lb 113.8 120.6 34.8 54.88 24.12 72 5 Rt hd lb 110.3 108 33.7 51.3 25.3 75

3.Alcohol extract treated (G3)

6 Lt hd lb 102.3 130 40.5 53 26.3 66 1 Head 119.3 121.1 34.3 57.64 27.3 66.3 2 Body 120.2 123.5 32.9 64.66 27.64 68.5 3 Tail 115.3 142 31.7 69.4 28.4 70.5 4 Rt ft lb 120.8 130.7 35.6 59.06 26.14 71 5 Rt hd lb 113.9 120.7 34.3 53 26.6 65.8

4.Chitrak churna treated (G4)

6 Lt hd lb 115.7 129.5 38.1 51.7 25.1 66 1 Head 108.7 112.9 38.7 44.21 24.5 70.8 2 Body 111.9 120.2 37.5 48.45 25.94 72 3 Tail 105 112.7 39.89 39.48 25.72 69.7 4 Rt ft lb 99.5 119.7 35.3 40.28 23.92 71.5 5 Rt hd lb 120.25 106.2 40.9 52.09 22.8 73.3

5.Standard drug (G5)

6 Lt hd lb 110.9 103.8 36.3 50 24.6 68.5 1 Head 90.4 123.6 40.8 24.88 24.72 60.8 2 Body 86.7 104.8 39.5 26.24 20.96 64

6.Chitraka churna to

normolipid 3 Tail 95.8 120.9 43.3 28.32 24.18 62



4 Rt ft lb 103.5 127.3 38.7 39.34 25.46 58 5 Rt hd lb 111.2 125 38.6 47.6 25 59 6 Lt hd lb 89.5 111.7 41 26.16 22.34 61

Table 4.4 showing master chart

Parameter 1.1- Total cholesterol

Table 4.5 showing the values of Total cholesterol (Mg/dl) of all the groups of rats

Samples Normal control

(G1)

Hyper lipid control

(G2)

Alcohol extract

(G3)

Chitrak churna

(G4)

Standard drug (G5)

Chitraka churna to

normolipid (G6)

1 89.5 140.5 108.4 119.3 108.7 90.4 2 96.3 138.3 118.7 120.2 111.9 86.7 3 87.1 122.7 109.2 115.3 105 95.8 4 90.5 143.3 113.8 120.8 99.5 103.5 5 106 130 110.3 113.9 120.25 111.2 6 79 151.7 102.3 115.7 110.9 89.5

Table 4.6 Summary of Data

S.L.No

Groups Samples Mean Standard Deviation

Standard Error of Mean

Median

1 Normalcontrol (G1) 6 91.4 9.098 3.714 90.00 2 Hyperlipidcontrol(G2) 6 137.75a 10.196 4.163 139.4 3 Alcohol extract (G3) 6 110.45*** 5.504 2.247 109.75 4 Chitrak churna (G4) 6 117.53** 2.914 1.190 117.50 5 Standard drug(G5) 6 109.37*** 6.971 2.846 109.8 6 Chitraka churna to

normolipid (G6) 6 96.183 9.458 3.861 93.1

a P < 0.001 compared with normal

*** P < 0.001, ** P < 0.01 compared with hyperlipidaemic control.

Graph 1

Mean values of Total cholesterol of all groups

0

20

40

60

80

100

120

140

Group 1

Group 2

Group 3

Group 4

Group 5

Group 6



Table 4.7 ANOVA Table

S.L.No

Source of variation

Degree of freedom

Sum of squares

Mean squares

F Value

1 Treatment 5 8178.5 1635.7 2 Residuals 30 1817.8 60.595 3 Total 35 9996.3 26.994

Results:

Administration of hydrocortisone to rats had produced an extremely significant

(P<0.001) increase in the levels of cholesterol (137.75 ± 4.16).

Alcoholic extract of Chitraka (110.4 ± 2.2) and standard drug treated (109.3±

2.8)) groups had high significantly reversed these variations.

Chitraka churna (117.5 ±1.19) had medium significantly reversed these variations.

Parameter 1.2 – Triglyceride

Table No 4.8 showing the values of Triglyceride (Mg/dl) of all the groups of rats


(G1)

Hyperlipid control (G2)

Alcohol extract

(G3)

Chitrak churna

(G4)

Standard drug (G5)

Chitraka churna to

normolipid (G6)

1 120 155.3 123.8 121.1 112.9 123.6 2 115 148 114.7 123.5 120.2 104.8 3 106.8 130 124.5 142 112.7 120.9 4 110 160.5 120.6 130.7 119.7 127.3 5 125 143.3 108 120.7 106.2 125 6 104.7 183.3 130 129.5 103.8 111.7



Table No. 4.9 Summary of Data

S.L.No


Standard Error of

Mean

Median

1 Normalcontrol (G1) 6 113.58 7.89 3.22 112.5 2 Hyperlipidcontrol(G2) 6 153.4a 18.03 7.36 151.65 3 Alcohol extract (G3) 6 120.27*** 7.83 3.19 122.2 4 Chitrak churna (G4) 6 127.92** 8.08 3.3 126.5 5 Standard drug(G5) 6 115.8*** 6.27 2.56 116.25 6 Chitraka churna to

normolipid (G6) 6 118.89 8.76 3.58 122.25


*** P < 0.001, ** P < 0.01 compared with hyperlipidaemic control.

Graph 2

Mean values of Triglyceride of all groups

TableNo 4.10 Anova Table

S.L.No

Source of variation

Degree of freedom

Sum of squares

Mean squares

F Value

0

20

40

60

80

100

120

140

160

Group 1

Group 2

Group 3

Group 4

Group 5

Group 6




Results:


(P<0.001) increase in the levels of triglycerides. (153.4±7.36)

Alcoholic extract of Chitraka (120.27± 3.19) and standard drug treated (115.3±

2.56) groups had high significantly reversed these variations.

Chitraka churna (127.9 ±3.3) had medium significantly reversed these variations.

Parameter 1.3 - HDL-C

Table No 4.11 showing the values of HDL-C (Mg/dl) of all the groups of rats


(G1)

Hyper lipid control

(G2)

Alcohol extract

(G3)

Chitrak churna

(G4)

Standard drug (G5)

Chitraka churna to

normolipid (G6)

1 40.5 31.5 38.4 34.3 38.7 40.8 2 42.8 31.8 36.6 32.9 37.5 39.5 3 39.3 33.4 33.35 31.7 39.89 43.3 4 41.2 30.8 34.8 35.6 35.3 38.7 5 36.7 29.5 33.7 34.3 40.9 38.6 6 37.2 32.4 40.5 38.1 36.3 41


S.L.No


Standard Error of

Mean

Median

1 Normalcontrol (G1) 6 39.617 2.361 0.963 39.9 2 Hyperlipidcontrol(G2) 6 31.567 a 1.34 0.546 31.65



0

5

10

15

20

25

30

35

40

Group 1

Group 2

Group 3

Group 4

Group 5

Group 6

3 Alcohol extract (G3) 6 36.883*** 1.508 0.615 36.7 4 Chitrak churna (G4) 6 35.567** 1.379 0.563 35.25 5 Standard drug(G5) 6 38.083*** 2.123 0.866 38.1 6 Chitraka churna to

normolipid (G6) 6 37.517 1.155 0.471 37.75


*** P < 0.001, ** P < 0.01 compared with hyperlipidaemic control

Graph 3

Mean values of HDL-C of all groups


S.L.No

Source of variation

Degree of freedom

Sum of squares

Mean squares

F Value


Results:


(P<0.001) decrease in the levels of HDL-C. (31.56±0.54)

Alcoholic extract of Chitraka (36.8± 0.61) and standard drug treated (38±0.86)

groups had high significantly reversed these variations.



Chitraka churna (35.56±0.56) had medium significantly reversed these variations.

Parameter 1.4 – LDL-C

Table No 4.14 showing the values of LDL-C (Mg/dl) of all the groups of rats


(G1)

Hyper lipid control

(G2)

Alcohol extract

(G3)

Chitrak churna

(G4)

Standard drug (G5)

Chitraka churna to

normolipid (G6)

1 22 77.9 57.2 57.64 44.21 24.88 2 30.5 76.9 57.8 64.66 48.45 26.24 3 26.44 63.3 50.95 69.4 39.48 28.32 4 27.3 80.4 54.88 59.06 40.28 39.34 5 44.3 71.84 51.3 53 52.09 47.6 6 21 82.64 53 51.7 50 26.16


S.L.No


Standard Error of Mean

Median

1 Normalcontrol (G1) 6 28.67 8.38 3.422 26.87 2 Hyperlipidcontrol(G2) 6 75.49 a 6.99 2.837 77.4 3 Alcohol extract (G3) 6 56.19*** 4.32 1.764 55.274 4 Chitrak churna (G4) 6 59.24** 6.79 2.77 58.35 5 Standard drug(G5) 6 45.75*** 5.23 2.13 46.33 6 Chitraka churna to

normolipid (G6) 6 32.09 9.26 3.78 27.28


*** P < 0.001, ** P < 0.01 compared with hyperlipidaemic control

Graph 4



Mean values of LDL-C of all groups


S.L.No

Source of variation

Degree of freedom

Sum of squares

Mean squares

F Value

1 Treatment 5 9398.3 1879.7 2 Residuals 30 1486.6 49.552 3 Total 35 10886 37.933

Results:


(P<0.001) increase in the levels of LDL-C. (75.4±2.83)

Alcoholic extract of Chitraka (56.1± 1.76) and standard drug treated

(45.754±2.13) groups had high significantly reversed these variations.

Chitraka churna (59.24±2.7) had medium significantly reversed these variations.

Parameter 1.5 – VLDL-C

Table No 4.17 showing the values of VLDL-C (Mg/dl) of all the groups of rats


(G1)

Hyperlipid control

(G2)

Alcohol extract

(G3)

Chitrak churna

(G4)

Standard drug (G5)

Chitraka churna to

normolipid (G6)

1 24 31.06 27.2 27.3 24.5 24.72 2 23 29.6 24.2 27.64 25.94 20.96

0

10

20

30

40

50

60

70

80

Group 1

Group 2

Group 3

Group 4

Group 5

Group 6



3 21.36 26 24.9 28.4 25.72 24.18 4 22 32.1 24.12 26.14 23.92 25.46 5 25 28.66 25.3 26.6 22.8 25 6 22.8 36.66 26.3 25.1 24.6 22.34


S.L.No


Standard Error of

Mean

Median

1 Normalcontrol (G1) 6 23.02 1.32 0.53 32.9 2 Hyperlipidcontrol(G2) 6 30.68 a 3.6 1.47 30.33 3 Alcohol extract (G3) 6 25.35*** 1.2 0.48 25.1 4 Chitrak churna (G4) 6 26.85* 1.17 0.48 26.95 5 Standard drug(G5) 6 24.58*** 1.16 0.47 24.55 6 Chitraka churna to

normolipid (G6) 6 23.77 1.75 0.71 24.45


*** P < 0.001, ** P < 0.01, * P < 0.05 compared with hyperlipidaemic control

Graph 5

Mean values of VLDL-C of all groups

0

5

10

15

20

25

30

35

Group 1

Group 2

Group 3

Group 4

Group 5

Group 6




S.L.No

Source of variation

Degree of freedom

Sum of squares

Mean squares

F Value


Results:


(P<0.001) increase in the levels of VLDL-C. (30.6±1.47)

Alcoholic extract of Chitraka (25.35±0.48) and standard drug treated

(24.58±0.47) groups had high significantly reversed these variations.

Chitraka churna (26.85±0.48) had less significantly reversed these variations

Parameter 2 - Serum glucose

Table No 4.20 showing the values of Serum glucose level (Mg/dl) of all the groups of

rats


(G1)

Hyper lipid control

(G2)

Alcohol extract

(G3)

Chitrak churna

(G4)

Standard drug (G5)

Chitraka churna to

normolipid (G6)

1 62.8 79.6 67.5 66.3 70.8 60.8 2 65.1 81.2 70.3 68.5 72 64 3 59 78.5 69 70.5 69.7 62 4 64 77.9 72 71 71.5 58 5 56 88 75 65.8 73.3 59 6 66.5 85.5 66 66 68.5 61



Table No 4.21 Summary of Data

S.L.No


Standard Error of

Mean

Median

1 Normalcontrol (G1) 6 62.23 3.97 1.62 63.4 2 Hyperlipidcontrol(G2) 6 81.78 a 4.08 1.66 80.4 3 Alcohol extract (G3) 6 65.8*** 3.49 1.42 69.65 4 Chitrak churna (G4) 6 68.01*** 2.33 0.95 67.4 5 Standard drug(G5) 6 70.96*** 1.7 0.69 71.15 6 Chitraka churna to

normolipid (G6) 6 60.8 2.13 0.87 60.9


*** P < 0.001 compared with hyperlipidaemic control

Graph 6

Mean values of Serum glucose of all groups


S.L.No

Source of variation

Degree of freedom

Sum of squares

Mean squares

F Value

1 Treatment 5 1691 338.27 2 Residuals 30 288.24 9.808 3 Total 35 1979.6 35.206

Results:


0

10

20

30

40

50

60

70

80

90

Group 1

Group 2

Group 3

Group 4

Group 5

Group 6



(P<0.001) increased in the levels of serum glucose. (81.78±1.66)

Alcoholic extract of Chitraka (65.8±1.42) and standard drug treated (70.96±0.69)

Chitraka churna (68.01±0.95) groups had highly significantly reversed these

variations.

Table 4.23 showing comparison of mean values of lipid levels between normal


Graph 7

0

20

40

60

80

100

120

140

160

T. Cholest Trigly HDL LDL VLDL

Group 1

Group 2

Table 4.24 showing comparison of mean values of lipid levels in between


Groups Cholesterol Triglyceride HDL-C LDL-C VLDL-C

Group 1 91.4 113.58 39.61 28.67 23.02

Group 2 137.75 153.4 31.56 75.49 30.68


Group 2 137.75 153.4 31.56 75.49 30.68

Group 3 110.45 120.27 36.8 56.19 25.85



Graph 8

0

20

40

60

80

100

120

140

160


Group 2

Group 3



Graph 9

0

20

40

60

80

100

120

140

160


Group 2

Group 4




Group 2 137.75 153.4 31.56 75.49 30.68

Group 4 117.5 127.92 35.56 59.26 26.85


Group 2 137.75 153.4 31.56 75.49 30.68

Group 5 109.37 118.89 37.51 32.09 23.77



Graph 10

0

20

40

60

80

100

120

140

160


Group 2

Group 5

Table 4.27 showing comparison of mean values of lipid levels in between normal


Graph 11

0

20

40

60

80

100

120

T.Cholest

Trigly HDL LDL VLDL

Group 1

Group 6


hyperlipidemic control and alcoholic extract, churna and standard drug treated grp.


Group 1 91.4 114.5 39.8 28.6 23.02 Group 6 96.18 118.89 37.51 32.09 23.37


Group 2 137.75 153.4 31.56 75.49 30.68

Group 3 110.45 120.27 36.8 56.19 25.85

Group 4 117.5 127.92 35.56 59.26 26.85

Group 5 109.37 118.89 37.51 32.09 23.77



Graph 12

0

20

40

60

80

100

120

140

160


Group 2

Group 3

Group 4

Group 5



Table No 4.29 Mean of all the groups for lipid levels

Groups Total

Cholesterol

(Mean ± SEM)

Triglyceride

(Mean ± SEM)

HDL-C

(Mean ± SEM)

LDL-C

(Mean ±

SEM)

VLDL-C

(Mean ±

SEM)

Normal control (G1) 91.4±3.71 113.58±3.22 39.617±0.96 28.67±3.42 23.02±0.53

Hyperlipidcontrol(G2 137.7± 4.16a 153.4±7.36 a 31.567±0.34 a 75.49±2.85 a 30.68±1.47 a

Alcohol extract (G3) 110.45±2.24*** 120.27±3.19*** 36.88±0.61*** 56.19±1.76*** 25.35±0.48***

Chitraka churna (G4) 117.53±1.19** 127.92±3.3** 35.567±0.56** 59.24±2.77** 26.85±0.48*

Standard drug(G5) 109.37±2.84*** 115.8±2.56*** 38.083±0.86**.* 45.75±2.13*** 24.58±0.47***

Chitraka churna to

normolipid (G6)

96.183±3.86

118.89±3.58 37.517±0.47 32.09±3.78 23.77±0.71

Values are expressed in mg/dl, a P < 0.001 compared with normal, *** P < 0.001, ** P < 0.01,* P < 0.05 compared

with hyper lipid group. *** Highly significant, **Medium significant, *Less significant.



Table No 4.30 Mean of all the groups for serum glucose

Groups Sr. Glucose

(Mean ± SEM)

Normal control (G1) 62.23±1.62

Hyperlipid control (G2) 81.78±1.66 a

Alcohol extract (G3) 65.8±1.42***

Chitrak churna (G4) 68.01±0.95***

Standard drug (G5) 70.96±0.69***

Chitraka churna to normolipid (G6) 60.8±0.87

Values are expressed in mg/dl, a P < 0.001 compared with normal,

*** P < 0.001, compared with hyper lipid group.

*** Highly significant



Results of histopathology study of liver and aorta samples:

Results of Liver section:

Group G1 (Normal control): Liver sections of normal control rats showing: normal

hepatic cells with well preserved cytoplasm; well brought out central vein; prominent

nucleus and nucleolus.

Group G2 (Hyperlipidemic control): Liver section showing: massive fatty changes,

accumulation of triglycerides, and broad infiltration of the lymphocytes and kupffer cells

around the central vein.

Group G3 (Alcohol extract): Liver section, showing: well brought out normal hepatic

cells and central vein, prominent nucleus and nucleolus little accumulation of fatty

content.

Group G4 (Chitrak churna): Photomicrograph of liver section, showing central vein

surrounded by hepatocytes with sinusoidal dilatation with accumulated fatty content. No

hepatic necrosis was seen around central vein or in the central zone.

Group G5 (Standard drug): Liver section, showing: well brought out central vein,

hepatic cell with well preserved cytoplasm, prominent nucleus and nucleolus, no

accumulation fatty content.

Group G6 (Chitraka churna to normolipid): Liver section, showing: well brought out

central vein, hepatic cell with well preserved cytoplasm, prominent nucleus and

nucleolus, no accumulation of fatty content.



Results of Aorta section

Group G1 (Normal control): The intima is limited by a single layer of flattened

endothelial cells, the middle layer consists of smooth muscle cells and outer most layers

consists of connective tissue surrounding the vessel and normal lumen was found.

Group G2 (Hyperlipid control): Fibrous plagues and fibrosis, plaques showing

calcification and atheromatous or Fibro-fatty plaque.

Group G3 (Alcohol extract): All three layers are normal, normal lumen and diffuse

intima thickening

Group G4 (Chitrak churna): The atheroma is often extensive, with plaques developing

adjacent to the origin.

Group G5 (Standard drug): Fatty streaks, all three layers are normal, normal lumen

was found.

Group G6 (Chitraka churna to normolipid): All three layers are normal, normal lumen

and no accumulation of fatty content was found.

Discussion…


DISCUSSION

The present study was carried out to evaluate the hypolipidaemic effect of

Chitraka through experimental study on albino rats. The study is entitled as “Evaluation

of medohara (hypolipidaemic) effect of Chitraka (Plumbago zeylanica Linn.) - An

experimental study.”

About the drug Chitraka:

References of the drug Chitraka could not be traced out in Veda and Purana. It is

extensively used in Samhita kala in the treatement of various diseases. All most all

nighantukaras have also explained Chitraka with a variety of synonyms and its

gunakarma.

Chitraka has got chief synonym as Agni. It is also known with all the names of

fire. This refers towards Ushna veerya and corrosive nature of Chitraka. Some synonyms

of it like Phaati, Vyaala indicates towards it pharmacological actions. Chitraka name it

self indicates the beautiful flowering nature of the plant. This is the only name which

indicates its morphological structure. The synonym of Agni is also applied to few other

dravyas, the properties of which are similar to Agni. They are Bhallataka, Mayooraka,

Ajmoda, Methika etc.

There are differences of opinion regarding types of Chitraka. Vagbhata achaarya

mentioned three types i.e. Peeta which is regarded as yellow flowered, Sita, white colored

and Asita, blue colored type. Raja nighantukara has mentioned two varities of Chitraka

i.e. Shweta and Rakta Chitraka. Rakta Chitraka is considered to be more potent with its

properties than Shweta Chitraka and hence the few synonyms used in this context like

Atideepya, Dipyagni are confirmatory with this statement.

Discussion…


Nowadays three types are available. The white flowered variety is Shweta

Chitraka and found all over India easily. Second red flowered variety i.e. Rakta Chitraka

is obtainable in some parts of India. The third blue flowered; "Neel Chitraka" is very rare.

Shweta Chitraka botanically identified as Plumbago zeylanica, Rakta chitraka as P. rosea

and that of Neela Chitraka as P. capensis.

Rasapanchaka of Chitraka is Laghu, Ruksha and Ushna guna, Katu rasa, Katu

Vipaka and Ushna Veerya. It is regarded as Kapha Vata shamaka by most of the authors.

Kaiyadeva has different opinion regarding this. According to him it has got Tikta and

katu rasa and it is tridoshahara. He further explains that it acts as Kaphahara due to its

Katu rasa, due to Tikta rasa as Pittahara and as Vatahara due to its ushna guna.

Chitraka has got pharmacological actions like lekhana, bhedana, deepana,

paachana etc. So it is widely used in the treatment of Agnimandyajanita diseases like

Medoroga, Arsha, Grahani, Atisara, Udara, Shotha, Kushtha, Gulma, Shwitra etc. Lots of

therapeutic uses of Chitraka in combination with other drugs can be traced Out, but single

drug therapy with Chitraka is very rarely seen.

Several references are suggestive of use of Chitraka in the treatement of

Medoroga. Some of them are as follows,

Chitraka is one among the lekhaneeya dashemani group of drugs explained by

acharya Charak 144.

Sushrutacharya included it under Varunaadi gana, which is indicated for the treatment

of Medoroga 145.

Vangasen indicates Chitraka moola choorna along with madhu in the treatment of

Medoroga 146.

Discussion…


About the disease:

There are no references of a single disease entity that can be directly correlated to

hyperlipidaemia in Ayurveda. Most of the scholars have considered it under the heading

of Medoroga. Hyperlipidaemia is one of the most important risk factors for susceptibility

of coronary heart disease. It is well documented fact that a positive correlation exist

between blood lipid, particularly cholesterol and coronary vascular disease.

Hyperlipidaemia is an important yet modifiable risk factor of all lipid

abnormalities. Studies have shown that a reduction in plasma cholesterol does infact

reduce the risk of myocardial infarction. Overall, 1% reduction in plasma cholesterol

concentration in middle-aged men reportedly results in 2% reduction in the incidence of

coronary heart diseases. Keeping this motto in back ground present study is selected over

hyperlipidaemia.

Phytochemical analysis of Chitraka:

Preliminary phytochemical analysis of Chitraka in different extracts i.e., aqueous,

alcoholic and chloroform were carried. It reveals the presence of carbohydrates, proteins,

alkaloids, glycosides, tannin, flavonoids, saponins and steroids. Chitraka is especially

rich with the flavonoids, tannin, alkaloids and glycosides.

Experimental study:

i) Experimental model:

There are many different experimental models to evaluate the hypolipidaemic

effect of the drugs. Some of them are like Triton induced hyperlipidaemia, Sucrose high

fat diet induced hyperlipidaemia, athero diet and cholesterol induced hyperlipidaemia etc.

Discussion…


For this present study, glucocorticoid induced hyperlipidaemic experimental method was

selected as this method found to be more convenient.

Glucocorticoids are secreted by zona fasciculata cells of adrenal cortex. Several

stimulatory factors are responsible for the release of glucocorticoids. Sudden increase in

the serum cortisol levels causes hyperglycemia, hyperlipidaemia, electrolyte depletion

and hypertension 147.

Glucocorticoid excess is known to evoke plasma lipid elevation but the pattern of

changes appears to vary in several species 148. (Krausz Y, Bar-on H, Shafrir E).

Dexamethasone administration (10mg/kg body weight) is shown to lower the activities of

lecithin cholesterol acyl transeferace (LCAT) and hepatic lipoprotein lipase, there by

increasing triglyceride level, inducing imbalance in lipid metabolism and leading to

hyperlipidaemia in rats 149.(Kaur N.. Sharma N., Gupta A.K.) So this model was selected

to evaluate the hypolipidaemic effect of Chitraka in glucocorticoid induced

hyperlipidaemia and hyperglycemic model.

ii) Animal model:

There are references that the rats are regarded as the suitable animal model for the

evaluation of hypolipdaemic activity 150. Therefore rats were selected as the animal

model.

iii) Effective dose:

A pilot study was conducted to determine the therapeutic dose of alcoholic extract

of Chitraka as there were no model experimental studies and standards or prior literature

were available for the study. According to OECD 420 guidelines, the LD50 cut value is

considered as 2000mg/kg body weight and 1/10th of it is considered as safe dose.

Discussion…


Chitraka is having Ushna, Teekshna properties and so its standard dose 151

(according to API) for human being is considered as 1000-2000mg. So taking these

things in to consideration, 1/10th of 2000mg/kg body weight was decided as a safe dose

instead of 5000mg/kg body weight.

iv) Analysis of experimental results:

Albino rats are grouped into 6 groups, containing 6 animals in each group of either sex

weighing between 180-230gms.

Administration of glucocorticoid intraperitonially in albino rats resulted in highly

significant (P<0.001) elevation of cholesterol, triglyceride, LDL-C, VLDL-C, and

reduction in the levels of HDL-C. This establishes the efficacy of the experimental

protocol to induce hyperlipidemic condition.

Significant (P<0.001) elevation of serum glucose levels was also observed in

glucocorticoid administered animals.

Alcoholic extract of Chitraka, Chitraka churna and standard drug treated groups

significantly decreased the levels of cholesterol, triglyceride, LDL, VLDL and

increased the levels of HDL as compared to hyperlipidaemic control group.

Though, the fall in serum lipid levels of alcoholic extract of Chitraka was less than

that of standard drug treated group it was statistically non significant (P > 0.05)

Group 4th rats received Chitraka churna after induction of hyperlipidaemia. This was

to intend to compare the effect of Chitraka churna to that of alcoholic extract.

By statistical analysis it is evident that the hypolipidaemic effect of alcoholic extract

of Chitraka was more significant (P<0.001) when compared with that of Chitraka

churna group (P<0.01).

Discussion…


Chitraka churna was administered to the group 6th albino rats with out inducing

hyperlipidaemia with the intension of observing the effect of Chitraka in normolipid

animals.

Slight differences in the lipid levels were observed in between the normal control (G1)

group and 6th group animals, i.e., the group which received Chitraka churna with out

induced hyperlipidemia. But the difference was statistically non significant. (P > 0.05)

Highly significant (P<0.001) reduction in the levels of serum glucose was also

observed in Alcoholic extract of Chitraka, Chitraka churna and standard drug treated

groups when compared to hyperlipidaemic control group.

Probable mode of action of drug:

It is very difficult to explain the exact mode of action of drug. But on the basis of

certain principles and theories, an attempt has been made here to describe the probable

mode of action of Chitraka.

In the present study it has been observed that the effect of alcoholic extract of

Chitraka was more when compared with the Chitraka churna treated group. This may be

because, as the extracts of drugs contain major part of active constituents, it exhibits

quicker and potent action. Size of the particles is also the other factor which influenced

the action of these drugs. ‘Smaller the particle size, greater is the absorption’ is the

general rule of pharmacology. So the size of particles in the extract being much less

compared to churna, it helped in the fast and potent action extract.

According to Ayurveda:

According to Ayurveda, the phamacodynamics of a drug can be evaluated through its

panchabhautic constitution and rasapanchaka.

Discussion…


Chitraka has Vayu, Akasha, Agni mahaabhoota predominance. These are opposite to

gunas of Prithvi and Jala. Hence it will reduce the bhujalaadhika meda 152.

It is having Katu, Rooksha and Teekshna guna, Katu vipaka, Ushna veerya and

Kapha Vatahara property. According to Kaiyadeva it also has got Tikta rasa.

With its Katu, Tikta rasa it facilitates deepana, paachana action and helps in the

correction of medodhatwagnimandya. According to Charaka 153, Katu rasa posses

mamsa lekhan, kaphahara properties and Tikta rasa posses the lekhana, karshana,

rasa, meda, kleda, upashoshana properties. Katu rasa has also got sneha, meda, kleda

shoshana properties 154. These properties may help in curing Medoroga.

With its Rooksha guna, it does rasa shoshana and shodhana and in turn reduces the

over nourished medadhatu. With Ushna guna it does medoshoshana, medodravana

and removes the sanga. Laghu guna of it being opposite to guru guna of meda it helps

in medakshaya. With Teekshna guna it does medachhedana 155.

Ushna veerya and Katu vipaka of Chitraka helps in ama pachana and agni deepana.

This metabolic disease demands "Agnivriddhi", particularly at the level of Meda

dhatvagni. When any agni is not proper, dhatus are not produced properly. Improper

function of agni is the root cause for all disease. Chitraka with its deepana and

pachana action encounters dhatvagnimandya and potentiates the dhatvagnimandhya

and help in ama-pachana, there by alleviates aparipakwa dhatu and ama. That in turn

helps to form the dhatus in proper proportion with samyak qualities. Their by it

ensues Sarvadhatuposhana.

Discussion…


According to modern:

Hypolipidaemic effect of Chitraka probably results from the increased elimination of

cholesterol in the form of bile acids. Recent research has also shown that the animal

with plumbagin excreted more fecal cholesterol and phospholipids 156. Increased

stimulation of bile acid synthesis may lead to an increased utilization of cellular free

cholesterol and thus help in regulation of cholesterol.

A recent study shows that aqueous and alcoholic extracts of Chitraka to possess anti-

oxidant properties and inhibit lipid per oxidation. The presence of polyphenolic

compounds and flavonoids in these extracts of Chitraka may reduce the oxidation of

LDL-c. This may explain the probable mode of action of Chitraka as hypolipidaemic

drug 157. (Tilak Jai C et.)

Probucol, a hypolipidemic drug is a potent lipophilic antioxidant and the ability to

inhibit atherosclerosis has been attributed to its antioxidant properties. The flavonoids

present in Chitraka may be responsible for its antioxidant as well as hypolipidemic

action 158. However, specific experiments need to be designed to validate these

hypotheses.

Scope for future study…


SCOPE FOR FUTURE STUDY

The study was conducted with one experimental protocol i.e glucocorticoid

induced hyperlipidaemic model, other models like Triton induced, Sucrose high

fat diet induced, athero diet and cholesterol induced hyperlipidaemia models can

be tested.

Study can be carried out on transgenic rat models available for screening drugs

for hypolipidaemic activity.

Study can also be carried out on other animal models.

Further Chitraka can be undertaken for clinical research to assess the claim made

on it.

Higher Phyto chemical investigations are required for the confirmatory evaluation

of responsible phyto constituents contributing to hypolipidaemic action.

Chitraka can also be compared with other existing hypolipidemic drugs.

The present study, however, has not investigated the mechanism of

hypolipidaemic action of Chitraka. This should be explored further in future

studies.

Chitraka can also be tested for its possible hypoglycemic effect.

Conclussion…


CONCLUSION

The word Chitraka is not found in Vedic periods but since Samhita Period it has been

used in medicine. Ayurvedic Classics have described wide range of therapeutic

properties of the plant and have indicated in Medoroga, Arsha, Grahani, Udara,

Shoola, Kushta, Meha, Shwitra, Gulma etc.

Chitraka has Katu, Tikta rasa; Katu vipaka; Laghu, Ruksha, Ushna Guna; and Ushna

Veerya.

Botanical source of Chitraka is Roots of Plumbago zeylanica Linn. The root and root

bark of Plumbago species contains Plumbagin, which is therapeutically an important

alkaloiod.

In Ayurveda, there is no direct reference of a single disease entity that can be directly

correlated with the hyperlipidaemia. Most of the scholars have considered

hyperlipidaemia under the heading of Medoroga.

Medoroga is the produced as a result of medodhatvagnimandya and it is Vatakapha

pradhana vyadhi.

The phytochemical studies have revealed that the trial drug Chitraka is rich source of

alkaloids, flavonoids, glycoside and tannin.

Safe doseof alcohol extract is considered to be 200mg/kg body weight in albino

rats. Dose of the Chitraka churna is decided by referring the table of Paget and

Barnes (1964) as 180mg/kg body weight.

The trial drug is found to be free from any sort of side effects or toxic effects during

the experimental study.

Conclussion…


Alcohol extract of Chitraka showed more significant hypolipdaemic effect, when

compared to Chitraka churna.

It was also effective in reducing hyperglycemia, which was also induced by

hydrocortisone.

It also reduced tissue lipid content of liver and regressed atheroma and plaque

formation in aorta.

Chitraka with its deepana & pachana action encounters dhatvagnimandya &

potentiates the dhatvagni. That in turn helps to form the dhatus in proper proportion

with samyak qualities. Their by it ensues sarvadhatuposhana.

Chitraka is an effective hypolipidaemic drug which is established through this

experimental study using glucocorticoid induced hyperlipidaemic experimental

model.

Summary…


SUMMARY

The study entitled “Evaluation of medohara (hypolipidaemic) effect of Chitraka

(Plumbago zeyanica Linn.) - An experimental study” is summarized as follows.

Introduction:

This part reveals the need for the study, aims and objectives and hypothesis

behind selecting test drug and hypolipidaemic model for the present study.

Review of Literature:

Review of Literature is very much essential for the research programmer.

Therefore it includes botanical identity, varieties, micro & macroscopic observations

along with the chemical aspects of Chitraka. The literary review also deals with the

concept of Medoroga and lipids & hyperlipidaemia..

Methodology:

Deals with the preparation of churna and alcohol extracts of Chitraka. It includes

details about materials and methods of phytochemical analysis and the protocol of the

experiment. In the experimental study the drug Chitraka was screened for its

hypolipidaemic activity on albino rats by using glucocorticoid induced hyperlipidaemic

model. In this study 6 groups of 6 albino rats in each group were selected. 1st group

served as normal control, 2nd as hyperlipidaemic control, 3rd group treated with alcoholic

extract, 4th group treated with churna, 5th group treated with standard drug i,e Atorvastatin,

6th group was treated with Chitraka churna with out pre-treatement with glucocorticoid.

Results and observations:

The hypolipidaemic effect in each group was recorded at the end of the study. No

side effects or toxic effects were observed during the period of experimental study.

Summary…


Observations were recorded and the results were statistically analysed and the

significance was elicited using ANOVA followed by Tokey cramer multiple comparision

test.

Alcoholic extract of Chitraka, Chitraka churna and standard drug treated groups

significantly decreased the levels of cholesterol, triglyceride, LDL, VLDL and increased

the levels of HDL as compared to hyperlipidaemic control group.

Chitraka churna administered to normolipid rats did not shown statistically

significant changes when compared to normal control group.

It also reduced tissue lipid content of liver and regressed atheroma and plaque

formation in aorta.

Discussion and conclusion:

The discussion aspect of this work plays a vital role to find out the best usage of

the drug. Including future scope for the study, in all the angles conclusions have been

drawn on this work.

Thus the trial drug Chitraka was found to be an efficacious hypolipidaemic

screened under experimental study using glucocorticoid induced hyperlipidaemic model.

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