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184

CHAPTER-7

PLANT PROFILE AND EVALUATION OF ANTIEPILEPTIC ACTIVITY OF GOSSYPIUM HERBACEUM

S. No. Name of the Sub-Title Page No.

7.1 Taxonomy 186-186

7.2 Distribution 186-186

7.3 Description 186-187

7.4 Chemical constituents 187-188

7.5 Traditional uses 188-189

7.6 Previous Investigations 189-192

7.7

7.8

Reason for selection

Materials and methods

192-192

193-198

7.9 Results 198-225

7.10 Discussion 225 -229

185

Fig: 7.1. Gossypium herbaceum

Fig: 7.2. Gossypium herbaceum

186

7.1. Taxonomy

Kingdom : Plantae

Phyllum : Magnoliophyta

Class : Magnoliopsida

Order : Malvales

Family : Malvaceae

Genus : Gossypium

Species : herbaceum

Synonyms : Gossypium indicum, Gossypium hirsutum

Common name : Levant cotton

Vernacular names

Sanskrit : Karpas

Hindi : Kapas

Tamil : Parutti

Telugu : Paththi

7.2. Distribution

It is native to Indian subcontinent and the adjacent areas such as

Pakistan, Nepal and the South-West of China. It is a common shrub

found through out India and is distributed abundantly in North India

parts of Gujarat, West Bengal, Assam and Tamilnadu. Extensively

cultivated in fields and hillocks. The plant is known by various names

in different languages is as under.

7.3. Description

Perennial or annual shrub or subshrub upto 3 m tall, with few

branches and nearly all parts irregularly dotted with black oil glands;

187

stem thick and rigid, stem and branches hairy or glabrous. Twigs,

petioles and peduncles round, green, sparsely pilose conspicuously

gland-dotted but in some forms the stems, etc., become purple and

the dots inconspicuous. Leaves almost reniform, distinctly cordate-

auriculate, leathery, glabrescent on maturity, often prominently

reticulate, blade less than half cut into 3-5-7 lobes; the lobes broad,

ovate, rotund, suddenly acute or apiculate, irregular below thinly

pilose and with the sinuses thrown up in folds; stipules long, linear,

acuminate; glands on the veins below, sometimes appearing on more

than the central one. Bracteoles green, broadly ovate-rotund, obtuse,

only very slightly united but prominently cordate, gashed across the

top into 7-9 fairly long irregular teeth, which decrease right and left.

Inflorescence proliferous, forming many lateral spurs that carry two or

more flowers, sometimes almost becoming “clustered”; stipules of the

small leaves of the spurs elliptic acuminate. Flowers not very large but

about twice the length of the bracteoles, yellow with purple claws.

Calyx large, loose, undulate or with short rounded teeth.

7.4. Chemical constituents

Gossypium herbaceum plant is rich in resin, phenols, steroids,

carbohydrates and fixed oils. The chief constituents of seeds of

Gossypium herbaceum are gossypetin, gossypol, quercetin, betaine,

choline and salicylic acid.

Cotton seed oil is known as “naturally hydrogenated” because it

contains saturated fatty acids viz oleic, palmitic and stearic acids.

188

Bark contains starch and chromogen substances, glucose, a yellow

resin, fixed oil, little tannins and 6% of ash. Seeds contain 10-29% of

oil, albuminoids, nitrogenous substances from 18-25% and lignin 15-

25%. Roots and barks contain colourless acid, resin, dihydroxy

benzoic acid and phenols. Flowers mainly contain colouring matter, a

glucoside named gossypetin. Leaves contain gossypetin-8-rhamnoside

[168-169].

7.5. Traditional uses

Cotton seeds are used to treat epilepsy [22, 128]. The flowers are

sweet, cooling, tonic, galactogogue, remove biliousness and kapha,

allay thirst, dispel hallucinations and wandering of mind, restore

consciousness. A syrup is prescribed in all forms of insanity, in

hypochondria, a poultice is applied to burns, scalds, scabies. They are

used as analgesic and are good for all kinds of inflammation. The

leaves remove vata, enrich the blood, increase the flow of urine and

cure all ear troubles. The juice of the leaves is good in dysentery, the

leaves with oil are applied as a plaster to gouty joints. The seeds are

galactogogue, expectorant, laxative and aphrodisiac, used in orchitis.

All parts of plant are used in the treatment of skin disease, uterine

discharges, snake-bite and scorpion-sting.

In India, the cotton seeds are employed to procure abortion. They

are considered a nervine tonic and are given in headache. They are

used as a galactogogue. The herbaceous parts contain much mucilage

and are used as a demulcent. The juice of fresh leaves is considered

189

very efficacious in the treatment of snake-bite. The root and leaves are

recommended for the treatment of scorpion-sting.

In Annam, the flowers are given in amenorrhoea and

dysmenorrhoea. The oil from the seeds is applied to wounds and used

in scabies and herbs.

In North America, the root bark is used in large doses as an

abortifacient. The seeds are considered antidysenteric and

galactogogue. The juice of the leaves is administered as an emollient

in diarrhea and in mild forms of dysentery.

In South America, cotton seeds in the form of decoction are

employed in the treatment of intermittent fevers.

In Cambodia, every part of plant is used medicinally. The whole

plant is considered febrifuge. The flowers and leaves pectoral and

antiphlogistic, the roots astringent, antidysenteric, diuretic and

emollient [168].

7.6. Previous Investigations

• Shi and Zhang studied the antifertility effect of gossypol I and

effects of gossypol on androgen dependent organs of mice and

rats [129].

• Shandilya and Clarkson reported the antireproductive and

hypolipidaemic effect of gossypol in male cynomalgus monkey

(Macaca fascicularis) [170].

• Aitken et al., analysed the direct effects of gossypol on human

spermatozoa [171].

190

• Bai and Shi investigated the inhibition of T type Calcium

currents in mouse spermatogenic cells by gossypol [172].

• Li et al., proved that the aqueous extract of Gossypium

herbaceum showed significant antidepressant-like effect due to

activation of adenyl cyclase-cAMP pathway in signal

transduction system and hence protecting the neurons from the

lesion [173].

• Uawonggul et al., reported the activity of aqueous extract of

Gossypium herbaceum leaves against Heterometrus laoticus

scorpion venom activity on fibroblast cell lysis [174].

• Narasimha and coworkers reported the diuretic activity of

ethyl acetate and alcohol extract of Gossypium herbaceum

leaves in Albino rats. They reported that the diuretic effect was

comparable with that of the standard drug, Frusemide and the

alcoholic extract showed significant activity than the ethyl

acetate extract as a diuretic [175].

• Mi et al., investigated the in vitro and in vivo activities and

related mechanism of apogossypolone (ApoG2) alone or in

combination with adriamycin (ADM) against human hepato-

cellular carcinoma (HCC). They concluded that ApoG2 is a

potential non-toxic target agent that induces apoptosis by

upregulating Noxa. Simultaneously inhibiting anti-apoptotic

proteins and promoting the effect of chemotherapy agent ADM

in HCC [176].

191

• Chaturvedi and coworkers reported the antimicrobial activity

of flavonoids from in vitro tissue culture and seeds of Gossypium

herbaceum by adopting disc diffusion method. They reported

that flavanoids from Gossypium herbaceum showed

antimicrobial activity [177].

• Zaman et al., estimated the total phenolic content. Further

they evaluated invitro antioxidant activities of Gossypium

herbaceum by using the Folin-Ciocalteu method and DPPH

assay and reported that the plant possess antioxidant

properties [188].

• Feitosa and coworkers evaluated the acetylcholinesterase

inhibition activity of ethyl acetate and methanol extracts of

Gossypium herbaceum leaves by using a microplate assay and a

thin-layer chromatography (TLC) “in situ” assay based on the

Ellman assay and reported that the extracts exhibited

significant acetylcholinesterase inhibition activity [179].

• Khalid et al., proved the antiulcer activity of ethanol extract of

Gossypium herbaceum flowers using ethanol induced acute

gastric ulcers in rats. They reported that the antiulcer effect of

extract was indicated by the reduction in the ulcer index and

significant prevention of gastric mucosal damage induced by

ethanol which might be related to the tannins and flavonoids

present in the extract [180].

• Kumar et al., investigated the in-vitro antioxidant activity of

hydroalcohol extract of leaves of Gossypium herbaceum using

192

DPPH radical scavenging effect and reducing power assays.

They concluded that the DPPH radical scavenging effect and

reducing power of the extract was concentration dependent and

the extract was rich in flavanoids and phenolic compounds.

They also concluded that Gossypium herbaceum is a potential

source of antioxidants and thus could prevent many radical

diseases [26].

• Velmurugan et al., investigated the wound healing activity of

methanol extract of leaves of Gossypium herbaceum by excision

and incision wound model and dead space wound model in rats.

They reported that the activity is due to the presence of different

phytoconstituents like flavanoids, tannins etc [181].

• Velmurugan et al., investigated the wound healing activity of

ethanol and ethyl ether fractions of leaves of Gossypium

herbaceum by dexamethasone delayed wound healing model in

rats. They reported that combination of extract plus

dexamethasone and individual fractions significantly increased

the breaking strength and suggested that Gossypium herbaceum

have good anti-diabetic and immune-stimulant effects which

will helpful for fast healing of wounds in infectious and disease

condition like diabetes [182].

7.7. Reason for selection

Recent reports revealed that leaves of Gossypium herbaceum

contain antioxidants in good quantities [26]. Hence, present study

designed to evaluate the antiepileptic activity of various extracts

193

(petroleum ether, chloroform, ethanol, aqueous) of leaves of

Gossypium herbaceum by using three animal models involving

GABAergic neurotransmission i.e., Maximum electroshock (MES),

Pentylenetetrazole (PTZ) and Isoniazid (INH)-induced convulsions in

mice.

7.8. Materials and methods

7.8.1. Drugs and Chemicals

Isoniazid (S.D Fine-Chem. Ltd), Diazepam (Ranbaxy),

Phenobarbitone sodium (Bayer AG) and Pentylenetetrazole (Sigma

Aldrich Chemical Co.). All other chemicals used are of Merck, India

(LR grade).

7.8.2. Plant collection

The leaves of Gossypium herbaceum were collected from Nellutla,

Warangal, Andhra Pradesh, India. They were identified and

authenticated by Prof. V. S. Raju, department of Botany, Kakatiya

University. The plant specimen was deposited at Kakatiya University

Herbarium (KUW), Warangal with voucher number 1865.

7.8.3. Preparation of the extracts

The fresh leaves of Gossypium herbaceum were collected, shade

dried and were made in to coarse powder. Then extracts of petroleum

ether, chloroform, ethanol and water were prepared by following

maceration method [118].

194

7.8.4. Preliminary Phytochemical Studies

Different extracts of plant were subjected to qualitative chemical

tests for various phytoconstituents like alkaloids, carbohydrates,

flavonoids, lipids, proteins, saponins, steroids and tannins [119].

7.8.5. Pharmacological Investigations

7.8.5.1. Acute toxicity studies

The procedure adopted for the study was described in

4.7.5.2 [120].

7.8.5.2. Evaluation of Anti-epileptic activity

7.8.5.2.1. Maximum Electroshock (MES) in mice


4.7.5.3.1 [40]. Animals were put on following treatment schedule.

Table 7.1. Treatment schedule of Petroleum ether extract of

Gossypium herbaceum in MES model

S. No Group Treatment

1 IPGM DMSO

2 IIPGM PGH (10 mg/kg, p.o.)

3 IIIPGM PGH (30 mg/kg, p.o.)

4 IVPGM PGH (100 mg/kg, p.o.)

5 VPGM Diazepam (3 mg/kg, p.o.)

195

Table 7.2. Treatment schedule of Chloroform extract of Gossypium

herbaceum in MES model

Table 7.3. Treatment schedule of Ethanol extract of Gossypium


Table 7.4. Treatment schedule of Aqueous extract of Gossypium


7.8.5.2.2. Pentylenetetrazole (PTZ)-induced convulsions


4.7.5.3.2 [85]. Animals were put on following treatment schedule.


1 ICGM DMSO

2 IICGM CGH (10 mg/kg, p.o.)

3 IIICGM CGH (30 mg/kg, p.o.)

4 IVCGM CGH (100 mg/kg, p.o.)

5 VCGM Diazepam (3 mg/kg, p.o.)


1 IEGM DMSO

2 IIEGM EGH (10 mg/kg, p.o.)

3 IIIEGM EGH (30 mg/kg, p.o.)

4 IVEGM EGH (100 mg/kg, p.o.)

5 VEGM Diazepam (3 mg/kg, p.o.)


1 IAGM Distilled water

2 IIAGM AGH (10 mg/kg, p.o.)

3 IIIAGM AGH (30 mg/kg, p.o.)

4 IVAGM AGH (100 mg/kg, p.o.)

5 VAGM Diazepam (3 mg/kg, p.o.)

196


Gossypium herbaceum in PTZ model


herbaceum in PTZ model




1 IPGP DMSO

2 IIPGP PGH (10 mg/kg, p.o.)

3 IIIPGP PGH (30 mg/kg, p.o.)

4 IVPGP PGH (100 mg/kg, p.o.)

5 VPGP Phenobarbitone sodium (40 mg/kg, i.p.)


1 ICGP DMSO

2 IICGP CGH (10 mg/kg, p.o.)

3 IIICGP CGH (30 mg/kg, p.o.)

4 IVCGP CGH (100 mg/kg, p.o.)

5 VCGP Phenobarbitone sodium (40 mg/kg, i.p.)


1 IEGP DMSO

2 IIEGP EGH (10 mg/kg, p.o.)

3 IIIEGP EGH (30 mg/kg, p.o.)

4 IVEGP EGH (100 mg/kg, p.o.)

5 VEGP Phenobarbitone sodium (40 mg/kg, i.p.)

197



7.8.5.2.3. Isoniazid (INH)-induced convulsions

The procedure adopted for the study was described in 4.7.5.3.3

[121]. Animals were put on following treatment schedule.


Gossypium herbaceum in INH model


herbaceum in INH model


1 IAGP Distilled water

2 IIAGP AGH (10 mg/kg, p.o.)

3 IIIAGP AGH (30 mg/kg, p.o.)

4 IVAGP AGH (100 mg/kg, p.o.)

5 VAGP Phenobarbitone sodium (40 mg/kg, i.p.)


1 IPGI DMSO

2 IIPGI PGH (10 mg/kg, p.o.)

3 IIIPGI PGH (30 mg/kg, p.o.)

4 IVPGI PGH (100 mg/kg, p.o.)

5 VPGI Diazepam (4 mg/kg, i.p.)


1 ICGI DMSO

2 IICGI CGH (10 mg/kg, p.o.)

3 IIICGI CGH (30 mg/kg, p.o.)

4 IVCGI CGH (100 mg/kg, p.o.)

5 VCGI Diazepam (4 mg/kg, i.p.)

198





7.9. Results

7.9.1. Percentage yield of different extracts of Gossypium

herbaceum

After extraction with different solvents by maceration method, the

percentage yield was calculated. The percentage yield obtained for

petroleum ether extract-20.89, chloroform extract-17.42, ethanol

extract-31.65 and aqueous extract-16.12.

7.9.2. Preliminary Phytochemical Studies

Preliminary phytochemical studies indicated the presence of

various phytoconstituents like alkaloids, steroids, carbohydrates,


1 IEGI DMSO

2 IIEGI EGH (10 mg/kg, p.o.)

3 IIIEGI EGH (30 mg/kg, p.o.)

4 IVEGI EGH (100 mg/kg, p.o.)

5 VEGI Diazepam (4 mg/kg, i.p.)


1 IAGI Distilled water

2 IIAGI AGH (10 mg/kg, p.o.)

3 IIIAGI AGH (30 mg/kg, p.o.)

4 IVAGI AGH (100 mg/kg, p.o.)

5 VAGI Diazepam (4 mg/kg, i.p.)

199

tannins, flavanoids, lipids and proteins in various extracts of the

plants.

Table 7.13. Preliminary phytochemical studies

Phytoconstituents PGH CGH EGH AGH

Alkaloids -ve - ve + ve + ve

Steroids + ve + ve + ve - ve

Carbohydrates - ve - ve - ve + ve

Tannins - ve - ve + ve + ve

Flavonoids - ve + ve + ve - ve

Saponins - ve - ve - ve - ve

Lipids + ve + ve + ve - ve

Proteins - ve - ve - ve + ve

7.9.3. Pharmacological Investigations

7.9.3.1. Acute toxicity studies

In the acute toxicity studies, mortality was found at 1000mg/kg,

p.o. for all the different extracts of Gossypium herbaceum. All the four

extracts were found to be safe upto the dose of 600 mg/kg, p.o. Based

on the results of the study, three doses of the four extracts i.e., 10, 30

and 100 mg/kg, p.o. were selected for the evaluation of anti-epileptic

activity.

7.9.3.2. Evaluation of Antiepileptic activity

7.9.3.2.1. Anti-epileptic activity of Petroleum ether extract of

Gossypium herbaceum (PGH)

7.9.3.2.1.1. Maximal electroshock-induced convulsions in mice

The average time of onset, duration of THLE and percentages of

inhibition of convulsions were presented in Table 7.14.

200

Effect on onset time of convulsions

The onset time of THLE for control group mice was 1.26±0.08 sec.

PGH treated mice showed the onset time as 1.72±0.05, 2.13±0.07 and

3.54±0.18 sec (p<0.01) respectively at the doses of 10, 30 and 100

mg/kg, p.o. The standard group mice (diazepam 3 mg/kg, p.o.)

showed 3.79±0.32 sec (p<0.01).

Effect on duration of convulsions

The duration of THLE for control group mice is 91.44±0.16 sec.

Albino mice which received PGH showed the duration of 40.77±0.94,

35.61±0.97 and 32.21±0.10 sec (p<0.01) respectively at the doses of

10, 30 and 100 mg/kg, p.o. The standard group mice (diazepam, 3

mg/kg, p.o.) showed 34.02±0.16 sec (p<0.01).

The time of onset of THLE for the control group animals was very

less when compared to the extract and standard treated animals.

Duration of THLE for the control group animals was greater when

compared to the extract and standard treated animals. Albino mice

pretreated with PGH at the doses of 10, 30 and 100 mg/kg were

provided significant protection from convulsions induced by

electroshock method in a dose-dependent manner.

Percentage inhibition of convulsions

The percentage inhibition achieved in PGH treated animals were

55.41% (10 mg/kg), 61.05% (30 mg/kg) and 64.78% (100 mg/kg)

(p<0.01) respectively when compared to control group animals. Albino

mice pretreated with PGH exhibited significant anti-epileptic activity

201

and less percentage inhibition when compared to diazepam treated

mice (62.79%, p<0.01).

Table 7.14. Effect of PGH on maximal electroshock-induced

convulsions in mice

Group

(n=6)=

6)

Treatment Onset of

THLE (sec)

Duration of

THLE (sec)

Percentage

inhibition of

convulsions

IPGM DMSO 1.26±0.08 91.44±0.16 -

IIPGM PGH (10 mg/kg) 1.72±0.05** 40.77±0.94** 55.41**

IIIPGM PGH (30 mg/kg) 2.13±0.07** 35.61±0.97** 61.05**

IVPGM PGH (100 mg/kg) 3.54±0.18** 32.21±0.10** 64.78**

VPGM Diazepam (3 mg/kg) 3.79±0.32** 34.02±0.16** 62.79**

PGH: Petroleum ether extract of Gossypium herbaceum; Values were

mean±SD (n=6). Statistical significance was determined by ANOVA,

followed by Dunnett’s t test (n=6); **p<0.01 when compared to Group

IPGM (control).

0102030405060708090

100

Dur

atio

n of

TH

LE

(sec

)

Treatment

DMSO

PGH 10 mg/Kg

PGH 30 mg/Kg

PGH 100 mg/Kg

Diazepam 3 mg/Kg

Fig: 7.3. Effect of PGH on duration of maximal electroshock-induced

convulsions in mice. Values were mean±S.D (n=6).

202

505254565860626466

Perc

enta

ge in

hibi

tion

of

conv

ulsio

ns

Treatment

PGH 10 mg/Kg

PGH 30 mg/Kg

PGH 100 mg/Kg

Diazepam 3 mg/Kg

Fig: 7.4. Effect of PGH on maximal electroshock-induced convulsions

in mice.

7.9.3.2.1.2. Pentylenetetrazole (PTZ)-induced convulsions in mice

The average time of onset, duration of convulsions and percentages

of inhibition of convulsions were presented in Table 7.15.


The onset time of convulsions for control group mice was

7.43±0.11 min. Albino mice pretreated with PGH at the doses of 10,

30 and 100 mg/kg, p.o. exhibited the onset time as 12.12±0.59,

17.01±0.40 and 22.29±0.13 min (p<0.01) respectively. Mice which

received Phenobarbitone sodium (40 mg/kg, i.p.) showed onset time of

4.51±0.09 min (p<0.01).


The duration of convulsions for control group mice was 18.57±0.40

min. Mice pretreated with PGH at the doses of 10, 30 and 100 mg/kg,

p.o. exhibited the duration as 11.54±0.06, 7.59±0.24 and 3.00±0.24

203

min (p<0.01) respectively. Mice belonging to standard group

(Phenobarbitone sodium, 40 mg/kg, i.p.) showed 9.24±0.09 min

(p<0.01).

It has been found that the time of onset of convulsions for control

group animals was very less when compared to the animals treated

with extract and standard. Duration of convulsions for control group

animals was greater when compared to the extract and standard

treated animals. All the three doses of PGH provided significant

protection from convulsions induced by PTZ in a dose-dependent

manner.


The percentage inhibition achieved in animals which received PGH

were 37.86%, 59.13% and 83.85% (p<0.01) respectively at the doses of

10, 30 and 100 mg/kg when compared to control group animals. PGH

treated mice exhibited significant antiepileptic activity (p<0.01) and

more percentage inhibition at the dose of 100 mg/kg when compared

to Phenobarbitone sodium 40 mg/kg, i.p. (50.23%, p<0.01).

204

Table 7.15. Effect of PGH on Pentylenetetrazole (PTZ)-induced

convulsions in mice

Group

(n=6)=

6)

Treatment

Onset of

convulsions

(min)

Duration of

convulsions

(min)

Percentage

inhibition of

convulsions

IPGP DMSO 7.43±0.11 18.57±0.40 -

IIPGP PGH (10 mg/kg) 12.12±0.59** 11.54±0.06** 37.86**

IIIPGP PGH (30 mg/kg) 17.01±0.40** 7.59±0.24** 59.13**

IVPGP PGH (100 mg/kg) 22.29±0.13** 3.00±0.24** 83.85**

VPGP Phenobarbitone sodium

(40 mg/kg, i.p.) 4.51±0.09** 9.24±0.09** 50.23**




IPGP (control).

02468

101214161820

Dur

atio

n of

con

vulsi

ons (

min

)

Treatment

DMSO

PGH 10 mg/Kg

PGH 30 mg/Kg

PGH 100 mg/Kg

Phenobarbitone sodium 40 mg/Kg

Fig: 7.5. Effect of PGH on duration of pentylenetetrazole-induced


205

0102030405060708090

Perc

enta

ge in

hibi

tion

of

conv

ulsi

ons

Treatment

PGH 10 mg/Kg

PGH 30 mg/Kg

PGH 100 mg/Kg


Fig: 7.6. Effect of PGH on pentylenetetrazole-induced convulsions in

mice.

7.9.3.2.1.3. Isoniazid (INH)-induced convulsions in mice

The average latency of convulsions were presented in Table 7.16.

Effect on latency of convulsions

The latency of convulsions in control group mice was 25.21±0.35

min. Albino mice pretreated with PGH showed the latency of

convulsions of 32.02±0.22, 37.55±0.04 and 43.12±0.04 min (p<0.01)

respectively at the doses of 10, 30 and 100 mg/kg, p.o. The standard

group mice (diazepam 4 mg/kg, i.p.) showed 63.27±0.13 min (p<0.01).

It has been found that the latency of convulsions for the control

group animals was very less when compared to the extract and

standard treated animals. Animals pretreated with all the three doses

of extract showed the latency time more than that of control group

animals and less than that of standard group animals i.e., diazepam.

It has been found that all the three doses of PGH significantly delayed

206

the latency of convulsions in mice but failed to protect the mice

against mortality.

Table 7.16. Effect of PGH on Isoniazid (INH)-induced convulsions in

mice

Group (n=6) Treatment Latency of convulsions (min)

I PGI DMSO 25.21±0.35

IIPGI PGH (10 mg/kg) 32.02±0.22**

III PGI PGH (30 mg/kg) 37.55±0.04**

IV PGI PGH (100 mg/kg) 43.12±0.04**

V PGI Diazepam (4 mg/kg, i.p.) 63.27±0.13**




IPGI (control).

010203040506070

Late

ncy

of c

onvu

lsion

s (m

in)

Treatment

DMSO

PGH 10 mg/Kg

PGH 30 mg/Kg

PGH 100 mg/Kg

Diazepam 4 mg/Kg

Fig: 7.7. Effect of PGH on isoniazid-induced convulsions in mice.

Values were mean±S.D (n=6).

207

7.9.3.2.2. Anti-epileptic activity of Chloroform extract of

Gossypium herbaceum (CGH)





The onset time of THLE for control group animals was 1.35±0.04

sec. CGH treated animals exhibited the onset time as 1.89±0.06,

2.61±0.19 and 3.76±0.05 sec (p<0.01) respectively at the doses of 10,

30 and 100 mg/kg, p.o. The standard group animals (diazepam 3



The duration of THLE for control group animals was 118.91±1.99

sec. Albino mice pretreated with CGH showed the duration of

49.24±0.85, 43.78±0.56 and 37.64±0.73 sec (p<0.01) respectively at

the doses of 10, 30 and 100 mg/kg, p.o. The standard group animals

(diazepam 3 mg/kg, p.o.) showed 49.37±0.74 sec (p<0.01).

The time of onset of THLE in control group animals was very less

when compared to the extract and standard treated animals. Duration

of THLE in control group animals was greater when compared to the

extract and standard treated animals. Albino mice pretreated with

CGH at the doses of 10, 30 and 100 mg/kg were provided significant

protection from convulsions induced by electroshock method.

208


The percentage inhibition achieved in CGH treated animals were

58.59%, 63.18% and 68.35% (p<0.01) respectively at the doses of 10,

30 and 100 mg/kg when compared to control group animals. CGH

treated mice exhibited significant and dose-dependent antiepileptic

activity and more percentage inhibition at both the doses of 30 and

100 mg/kg when compared to diazepam treated mice (58.48%,

p<0.01).

Table 7.17. Effect of CGH on maximal electroshock-induced

convulsions in mice

Group

(n=6)=

6)

Treatment Onset of

THLE (sec)

Duration of

THLE (sec)

Percentage

inhibition of

convulsions

ICGM DMSO 1.35±0.04 118.91±1.99 -

IICGM CGH (10 mg/kg) 1.89±0.06** 49.24±0.85** 58.59**

IIICGM CGH (30 mg/kg) 2.61±0.19** 43.78±0.56** 63.18**

IVCGM CGH (100 mg/kg) 3.76±0.05** 37.64±0.73** 68.35**

VCGM Diazepam (3 mg/kg) 2.46±0.08** 49.37±0.74** 58.48**

CGH: Chloroform extract of Gossypium herbaceum; Values were



ICGM (control).




209


The onset time of convulsions for control group animals was

7.43±0.11 min. Animals pretreated with CGH at the doses of 10, 30

and 100 mg/kg, p.o. exhibited the onset time as 14.47±0.08,

19.34±0.07 and 24.46±0.07 min (p<0.01) respectively. Albino mice

pretreated with Phenobarbitone sodium, 40 mg/kg, i.p. showed onset

time as 4.51±0.09 min (p<0.01).


The duration of convulsions in control group animals was

18.57±0.40 min. CGH received animals exhibited the duration as

11.05±0.24 (10 mg/kg), 7.04±0.03 (30 mg/kg) and 2.51±0.05 min

(100 mg/kg) (p<0.01) respectively. Animals belonging to standard

group (Phenobarbitone sodium, 40 mg/kg, i.p.) showed 9.24±0.09 min

(p<0.01).

The time of onset of convulsions in control group animals was very

less when compared to the extract and standard group animals.

Duration of convulsions in control group animals was greater when

compared to the extract and standard group animals. All the three

doses of CGH significantly protected the mice against convulsions

induced by PTZ in a dose-dependent manner.


The percentage inhibition achieved in animals pretreated with CGH


10, 30 and 100 mg/kg when compared to control group animals.

Animals which received CGH exhibited significant and dose-dependent

210

antiepileptic activity and more percentage inhibition of convulsions at

both the doses of 30 and 100 mg/kg when compared to

Phenobarbitone sodium 40 mg/kg, i.p. (50.23%, p<0.01).

Table 7.18. Effect of CGH on Pentylenetetrazole (PTZ)-induced

convulsions in mice

Group

(n=6)) Treatment

Onset of

convulsions

(min)

Duration of

convulsions

(min)

Percentage

inhibition of

convulsions

ICGP DMSO 7.43±0.11 18.57±0.40 -

IICGP CGH (10 mg/kg) 14.47±0.08** 11.05±0.24** 40.53**

IIICGP CGH (30 mg/kg) 19.34±0.07** 7.04±0.03** 62.09**

IVCGP CGH (100 mg/kg) 24.46±0.07** 2.51±0.05** 86.49**

VCGP Phenobarbitone sodium

(40 mg/kg, i.p.) 4.51±0.09** 9.24±0.09** 50.23**




ICGP (control).




The latency of convulsions in control group animals was

25.21±0.35 min. Albino mice pretreated with CGH showed the latency

of convulsions of 32.03±0.24, 37.55±0.04 and 43.12±0.03 min

(p<0.01) respectively at the doses of 10, 30 and 100 mg/kg, p.o. The

standard group mice (diazepam 4 mg/kg, i.p.) showed 63.27±0.13 min

(p<0.01).

211

The latency of convulsions in control group animals was very less

when compared to the extract and standard group animals. All the

three doses of CGH showed the latency time more than that of control

group animals and less than that of standard group animals i.e.,

diazepam. It has been found that all the three doses of CGH

significantly delayed the latency of convulsions in mice but failed to

protect the mice against mortality.

Table 7.19. Effect of CGH on Isoniazid (INH)-induced convulsions in

mice

Group(n=6) Treatment Latency of

convulsions (min)

ICGI DMSO 25.21±0.35

IICGI CGH (10 mg/kg) 32.03±0.24**

IIICGI CGH (30 mg/kg) 37.55±0.04**

IVCGI CGH (100 mg/kg) 43.12±0.03**

VCGI Diazepam (4 mg/kg, i.p.) 63.27±0.13**




ICGI (control).

7.9.3.2.3. Anti-epileptic activity of Ethanol extract of Gossypium

herbaceum (EGH)




212


The onset time of THLE for control group mice was 1.35±0.04 sec.

EGH treated mice showed the onset time as 1.96±0.11, 2.66±0.05 and

4.62±0.05 sec (p<0.01) respectively at the doses of 10, 30 and 100

mg/kg, p.o. The standard group mice (diazepam 3 mg/kg, p.o.)

showed 2.46±0.08 sec (p<0.01).


The duration of THLE for control group mice is 118.91±1.99 sec.

Albino mice which received EGH showed the duration of 44.28±0.91,

38.38±0.91 and 32.06±0.59 sec (p<0.01) respectively at the doses of

10, 30 and 100 mg/kg, p.o. The standard group mice (diazepam 3


The time of onset of THLE for the control group animals was very

less when compared to the extract and standard treated animals.

Duration of THLE for the control group animals was greater when

compared to the extract and standard treated animals. Albino mice

pretreated with EGH at the doses of 10, 30 and 100 mg/kg were

provided significant protection from convulsions induced by

electroshock method in a dose-dependent manner.


The percentage inhibition achieved in animals which received EGH

were 62.76% (10 mg/kg), 67.72% (30 mg/kg) and 73.04% (100 mg/kg)

(p<0.01) respectively when compared to control group animals. EGH

treated animals exhibited significant and dose-dependent anti-

213

epileptic activity and less percentage inhibition when compared to

diazepam treated animals (58.48%, p<0.01).

Table 7.20. Effect of EGH on maximal electroshock-induced

convulsions in mice

Group

(n=6)=

6)

Treatment Onset of

THLE (sec)

Duration of

THLE (sec)

Percentage

inhibition of

convulsions

IEGM DMSO 1.35±0.04 118.91±1.99 -

IIEGM EGH (10 mg/kg) 1.96±0.11** 44.28±0.91** 62.76**

IIIEGM EGH (30 mg/kg) 2.66±0.05** 38.38±0.91** 67.72**

IVEGM EGH (100 mg/kg) 4.62±0.05** 32.06±0.59** 73.04**

VEGM Diazepam (3 mg/kg) 2.46±0.08** 49.37±0.74** 58.48**

EGH: Ethanol extract of Gossypium herbaceum; Values were mean±SD

(n=6). Statistical significance was determined by ANOVA, followed by

Dunnett’s t test (n=6); **p<0.01 when compared to Group IEGM

(control).





The onset time of convulsions for control group mice was

7.43±0.11 min. Albino mice pretreated with EGH at the doses of 10,

30 and 100 mg/kg, p.o. exhibited the onset time as 15.55±0.05,

20.59±0.22 and 25.51±0.25 min (p<0.01) respectively. Mice which

received Phenobarbitone sodium (40 mg/kg, i.p.) showed onset time of

4.51±0.09 min (p<0.01).

214


The duration of convulsions for control group mice was 18.57±0.40

min. Mice pretreated with EGH at the doses of 10, 30 and 100 mg/kg,

p.o. exhibited the duration as 10.05±0.31, 6.23±0.07 and 2.05±0.03

min (p<0.01) respectively. Mice belonging to standard group


(p<0.01).

It has been found that the time of onset of convulsions for control

group animals was very less when compared to the extract and

standard group animals. Duration of convulsions in control group


group animals. All the three doses of EGH provided significant

protection to mice from convulsions induced by PTZ in a dose-

dependent manner.


The percentage inhibition achieved in animals which received EGH


10, 30 and 100 mg/kg when compared to control group animals.

Albino mice pretreated with EGH exhibited significant and dose-

dependent antiepileptic activity (p<0.01) and more percentage

inhibition at both the doses of 30 mg/kg and 100 mg/kg when

compared to Phenobarbitone sodium 40 mg/kg, i.p. (50.23%, p<0.01).

215

Table 7.21. Effect of EGH on Pentylenetetrazole (PTZ)-induced

convulsions in mice

Group

(n=6)=

6)

Treatment

Onset of

convulsions

(min)

Duration of

convulsions

(min)

Percentage

inhibition of

convulsions

IEGP DMSO 7.43±0.11 18.57±0.40 -

IIEGP EGH (10 mg/kg) 15.55±0.05** 10.05±0.31** 45.87**

IIIEGP EGH (30 mg/kg) 20.59±0.22** 6.23±0.07** 66.48**

IVEGP EGH (100 mg/kg) 25.51±0.25** 2.05±0.03** 88.96**

VEGP Phenobarbitone sodium

(40 mg/kg, i.p.) 4.51±0.09** 9.24±0.09** 50.23**



Dunnett’s t test (n=6); **p<0.01 when compared to Group IEGP (control).




The latency of convulsions for control group mice was 25.21±0.35

min. Albino mice pretreated with EGH showed the latency of

convulsions of 35.44±0.02, 41.08±0.05 and 46.23±0.05 min (p<0.01)

respectively at the doses of 10, 30 and 100 mg/kg, p.o. The standard

group mice (diazepam 4 mg/kg, i.p.) showed 63.27±0.13 min (p<0.01).

The latency of convulsions for control group animals was very less

when compared to the extract and standard group animals. All the

three doses of EGH showed the latency time more than that of control

group animals and less than that of standard group animals i.e.,

diazepam. It has been found that all the three doses of EGH

216

significantly delayed the latency of convulsions in mice but failed to

protect the mice against mortality.

Table 7.22. Effect of EGH on Isoniazid (INH)-induced convulsions in

mice

Group (n=6) Treatment Latency of

convulsions (min)

IEGI DMSO 25.21±0.35

IIEGI EGH (10 mg/kg) 35.44±0.02**

IIIEGI EGH (30 mg/kg) 41.08±0.05**

IVEGI EGH (100 mg/kg) 46.23±0.05**

VEGI Diazepam (4 mg/kg, i.p.) 63.27±0.13**



Dunnett’s t test (n=6); **p<0.01 when compared to Group I EGI (control).

0

20

40

60

80

100

120

140

Dur

atio

n of

TH

LE (s

ec)

Treatment

DMSO

CGH 10 mg/Kg

CGH 30 mg/Kg

CGH 100 mg/Kg

EGH 10 mg/Kg

EGH 30 mg/Kg

EGH 100 mg/Kg

Diazepam 3 mg/Kg

Fig: 7.8. Effect of CGH and EGH on duration of maximal electroshock-

induced convulsions in mice. Values were mean±S.D (n=6).

217

01020304050607080

Perc

enta

ge in

hibi

tion

of

conv

ulsio

ns

Treatment

CGH 10 mg/Kg

CGH 30 mg/Kg

CGH 100 mg/Kg

EGH 10 mg/Kg

EGH 30 mg/Kg

EGH 100 mg/Kg

Diazepam 3 mg/Kg

Fig: 7.9. Effect of CGH and EGH on maximal electroshock-induced

convulsions in mice.

02468

101214161820

Dur

atio

n of

con

vuls

ions

(min

)

Treatment

DMSO

CGH 10 mg/Kg

CGH 30 mg/Kg

CGH 100 mg/Kg

EGH 10 mg/Kg

EGH 30 mg/Kg

Fig: 7.10. Effect of CGH and EGH on duration of pentylenetetrazole-

induced convulsions in mice. Values were mean±S.D (n=6).

218

0102030405060708090

100

Perc

enta

ge in

hibi

tion

of

conv

ulsi

ons

Treatment

CGH 10 mg/Kg

CGH 30 mg/Kg

CGH 100 mg/Kg

EGH 10 mg/Kg

EGH 30 mg/Kg

EGH 100 mg/Kg

Fig: 7.11. Effect of CGH and EGH on pentylenetetrazole-induced

convulsions in mice.

0

10

20

30

40

50

60

70

Lat

ency

of c

onvu

lsion

s (m

in)

Treatment

DMSO

CGH 10 mg/Kg

CGH 30 mg/Kg

CGH 100 mg/KgEGH 10 mg/Kg

EGH 30 mg/Kg

Fig: 7.12. Effect of CGH and EGH on isoniazid-induced convulsions in

mice. Values were mean±S.D (n=6).

219

7.9.3.2.4. Anti-epileptic activity of Aqueous extract of Gossypium

herbaceum (AGH)





The onset time of THLE for control group animals was 1.51±0.09

sec. AGH treated mice showed the onset time as 1.89±0.07, 3.32±0.13

and 5.06±0.11sec (p<0.01) respectively at the doses of 10, 30 and 100

mg/kg, p.o. The standard group animals (diazepam 3 mg/kg, p.o.)

showed 3.55±0.19 sec (p<0.01).


The duration of THLE for control group animals was 93.55±0.17

sec. AGH treated mice showed the duration of 43.66±0.06, 39.84±0.16

and 35.54±0.12 sec (p<0.01) respectively at the doses of 10, 30 and

100 mg/kg, p.o. The standard group animals (diazepam 3 mg/kg, p.o.)

showed 39.56±0.09 sec (p<0.01).

The time of onset of THLE in control group animals was very less

when compared to the extract and standard group animals. Duration

of THLE in control group animals was greater when compared to the

extract and standard group animals. Albino mice pretreated with AGH

at the doses of 10, 30 and 100 mg/kg were provided significant

protection from convulsions induced by electroshock method in a

dose-dependent manner.

220


The percentage inhibition achieved in animals pretreated with AGH


10, 30 and 100 mg/kg when compared to control group animals. AGH

treated animals exhibited significant and dose-dependent antiepileptic

activity and more percentage inhibition of convulsions at the dose of

100 mg/kg at the dose of 30 mg/kg when compared to diazepam 3.0

mg/kg (57.71%, p<0.01).

Table 7.23. Effect of AGH on maximal electroshock-induced

convulsions in mice

Group

(n=6)=

6)

Treatment Onset of

THLE (sec)

Duration of

THLE (sec)

Percentage

inhibition of

convulsions

IAGM Distilled water 1.51±0.09 93.55±0.17 -

IIAGM AGH (10 mg/kg) 1.89±0.07** 43.66±0.06** 53.33**

IIIAGM AGH (30 mg/kg) 3.32±0.13** 39.84±0.16** 57.42**

IVAGM AGH (100 mg/kg) 5.06±0.11** 35.54±0.12** 62.01**

VAGM Diazepam (3 mg/kg) 3.55±0.19** 39.56±0.09** 57.71**

AGH: Aqueous extract of Gossypium herbaceum; Values were mean ±

SD (n = 6). Statistical significance was determined by ANOVA, followed

by Dunnett’s t test (n=6); **p < 0.01 when compared to Group IAGM

(control).

221

0102030405060708090

100

Dur

atio

n of

TH

LE

(sec

)

Treatment

Distilled water

AGH 10 mg/Kg

AGH 30 mg/Kg

AGH 100 mg/Kg

Diazepam 3 mg/Kg

Fig: 7.13. Effect of AGH on duration of maximal electroshock-induced


485052545658606264

Perc

enta

ge in

hibi

tion

of

conv

ulsio

ns

Treatment

AGH 10 mg/Kg

AGH 30 mg/Kg

AGH 100 mg/Kg

Diazepam 3 mg/Kg

Fig: 7.14. Effect of AGH on maximal electroshock-induced convulsions

in mice.





222

The onset time of convulsions for control group mice was 7.51±0.05

min. Albino mice pretreated with AGH at the doses of 10, 30 and 100

mg/kg, p.o. exhibited the onset time as 13.35±0.05, 18.29±0.05 and

23.39±0.04 min (p<0.01) respectively. The standard group mice

(Phenobarbitone sodium, 40 mg/kg, i.p.) showed onset time as

4.49±0.04 min (p<0.01).


The duration of convulsions in control group animals was

19.23±0.07 min. Animals which received AGH exhibited the duration

as 12.47±0.04, 8.38±0.05 and 3.34±0.03 min (p<0.01) respectively at

the doses of 10, 30 and 100 mg/kg, p.o. The standard group animals


(p<0.01).

It has been found that the time of onset of convulsions for the

control group animals was very less when compared to the extract and

standard group animals. Duration of convulsions in control group


group animals. All three doses of AGH significantly protected the mice

from convulsions induced by PTZ in a dose-dependent manner.


Albino mice pretreated with AGH at the doses of 10, 30 and 100

mg/kg, p.o. exhibited the percentage inhibition of 35.14%, 56.41%

and 82.65% (p<0.01) respectively when compared to control group

animals. AGH treated animals exhibited significant and dose-

dependent antiepileptic activity more percentage inhibition at both the

223

doses of 30 and 100 mg/kg when compared to Phenobarbitone

sodium 40 mg/kg, i.p. (52.46%, p<0.01).

Table 7.24. Effect of AGH on Pentylenetetrazole (PTZ)-induced

convulsions in mice

Group

(n=6)=

6)

Treatment

Onset of

convulsions

(min)

Duration of

convulsions

(min)

Percentage

inhibition of

convulsions

IAGP Distilled water 7.51±0.05 19.23±0.07 -

IIAGP AGH (10 mg/kg) 13.35±0.05** 12.47±0.04** 35.14**

IIIAGP AGH (30 mg/kg) 18.29±0.05** 8.38±0.05** 56.41**

IVAGP AGH (100 mg/kg) 23.39±0.04** 3.34±0.03** 82.65**

VAGP Phenobarbitone sodium

(40 mg/kg, i.p.) 4.49±0.04** 9.14±0.04** 52.46**

AGH: Aqueous extract of Gossypium herbaceum; Values were

mean±SD (n = 6). Statistical significance was determined by ANOVA,

followed by Dunnett’s t test (n=6); **p < 0.01 when compared to Group

IAGP (control).

05

10152025

Dur

atio

n of

con

vulsi

ons (

min

)

Treatment

Distilled water

AGH 10 mg/Kg

AGH 30 mg/Kg

AGH 100 mg/Kg


Fig: 7.15. Effect of AGH on duration of pentylenetetrazole-induced


224

0102030405060708090

Perc

enta

ge in

hibi

tion

of

conv

ulsio

ns

Treatment

AGH 10 mg/Kg

AGH 30 mg/Kg

AGH 100 mg/Kg


Fig: 7.16. Effect of AGH on pentylenetetrazole-induced convulsions in

mice.




The latency of convulsions in control group animals was

24.14±0.04 min. Albino mice pretreated with AGH showed the latency

of convulsions of 29.55±0.03, 35.12±0.08 and 40.55±0.03 min

(p<0.01) respectively at the doses of 10, 30 and 100 mg/kg, p.o. The

standard group mice (diazepam 4 mg/kg, i.p.) showed 63.27±0.13 min

(p<0.01).

The latency of convulsions in control group animals was very less

when compared to the extract and standard group animals. AGH

treated animals showed the latency more than that of control group

animals and less than that of standard group animals i.e., diazepam.

It has been found that all the three doses of AGH significantly delayed

225

the latency of convulsions in mice but failed to protect the mice

against mortality.

Table 7.25. Effect of AGH on Isoniazid (INH)-induced convulsions in

mice

Group (n=6) Treatment Latency of

convulsions (min)

I AGI Distilled water 24.14±0.04

IIAGI AGH (10 mg/kg) 29.55±0.03**

IIIAGI AGH (30 mg/kg) 35.12±0.08**

IVAGI AGH (100 mg/kg) 40.55±0.03**

V AGI Diazepam (4 mg/kg, i.p.) 63.27±0.13**

AGH: Aqueous extract of Gossypium herbaceum; Values were


followed by Dunnett’s t test (n=6); **p<0.01 when compared to Group I

AGI (control).

010203040506070

Late

ncy

of c

onvu

lsion

s (m

in)

Treatment

Distilled water

AGH 10 mg/Kg

AGH 30 mg/Kg

AGH 100 mg/Kg

Diazepam 4 mg/Kg

Fig: 7.17. Effect of AGH on isoniazid-induced convulsions in mice.

Values were mean±S.D (n=6).

7.10. Discussion

Epilepsy is a serious neurological disorder, which does not have

any boundaries such as age, race, social class or nationality. The

226

incidence of the disease in developing countries is higher than that in

developed countries and is reported to be 57 per 1000.

Drug therapy of epilepsy with currently available anti-epileptic

drugs (AED) is associated with dose-related side effects and chronic

toxicity that involves virtually every organ system. It can be well

imagined that all the above mentioned problems with the current AED

therapy of epilepsy are more prevalent in underdeveloped countries

due to lack of facilities for proper diagnosis, treatment and monitoring

serum levels of AED.

Different types of epileptic seizures have varied susceptibility to

currently available AED and on the whole approximately two thirds of

the patients with epilepsy can have remission of seizures [44]. There is

a pressing need for further research in the field of pharmacotherapy of

epilepsy to find drugs with lesser adverse effects. Search for anti-

epileptic agents has made man turn to alternative sources i.e.,

exploitation of medicinal plants.

Earlier reports suggested that plants which are rich in antioxidant

principles eg: Crinum ornatum, Cyperus rotundus, Brassica nigra,

Ferula asafoetida, Astragalus mongolicus and Convolvulus pluricaulis

[82, 91, 101, 183-185] exhibited significant protection against

epilepsy. Gossypium herbaceum is one such plant which is enriched

with antioxidant principles [181-182]. Recent reports revealed that

leaves of Gossypium herbaceum also contain antioxidants in good

quantities [26]. Hence, present study designed to evaluate the

antiepileptic activity of various extracts of leaves of Gossypium

herbaceum.

227

Petroleum ether, chloroform, ethanol and aqueous extracts of the

tested plants were prepared to predict which phytoconstituents are

responsible for the remarkable antiepileptic activity.

Preliminary phytochemical studies indicated the presence of

various phytoconstituents like alkaloids, steroids, carbohydrates,

tannins, flavanoids, lipids and proteins in various extracts of the

plants.

In acute toxicity studies, all the extracts of this plant was found to

be safe upto 600 mg/kg, p.o. So, the doses of 10, 30, and 100 mg/kg,

p.o. were selected for all the extracts to evaluate antiepileptic activity.

The plant extracts were evaluated for antiepileptic activity by three

animal models in which GABAergic neurotransmission is involved viz.

MES, PTZ and INH models.

MES-induced convulsions are a suitable model for identifying

compounds/extracts effective in grand mal epilepsy [40]. In this test,

among all the tested extracts, ethanol extract of Gossypium

herbaceum (EGH) significantly inhibited MES-induced THLE to the

maximum extent at 100 mg/kg, dose (p.o.) with percentage of

inhibition of 73.04%. The order of antiepileptic activity for various

extracts of Gossypium herbaceum in MES model was

ethanol>chloroform>petroleum ether>aqueous (chloroform-68.35%,

petroleum ether-64.78% and aqueous-62.01%). As all the extracts

were protecting mice from MES-induced convulsions, they might

become useful in treating grand mal epilepsy. Maximum antiepileptic

activity of the ethanol extract might be due to the presence of phenolic

compounds such as flavanoids, tannins.

228

PTZ is a predictive model for identifying compounds/extracts

effective in treating petit mal epilepsy [40]. In this model, out of all the

tested extracts, ethanol extract significantly protected the mice

against PTZ-induced convulsions to the maximum extent at the dose

of 100 mg/kg, bd. wt dose (p.o.) with percentage of inhibition of

88.96% (chloroform-86.49%, petroleum ether-83.85%, aqueous-

82.65%). As all the extracts were effectively inhibiting PTZ-induced

convulsions, they might become useful in the treatment of petit mal

epilepsy. The presence of phenolic compounds such as flavanoids and

tannins in the ethanol extract might be responsible for the potent

activity.

Isoniazid lowers the brain GABA levels in humans to approximately

the same extent in rats and mice [32]. In INH model, all the extracts of

Gossypium herbaceum significantly delayed the latency of convulsions

in dose-dependent manner, maximum delay in latency of convulsions

was observed for ethanol extract at the dose of 100 mg/kg, p.o. But all

the extracts failed to protect the mice from mortality. Hence, the

extracts were unable to antagonize the action of INH.

All the extracts exhibited significant antiepileptic activity in all the

three models. The order of activity is AGH<PGH<CGH<EGH. Aqueous

extract of Gossypium herbaceum contains alkaloids, tannins,

carbohydrates and proteins which might be not sufficient for

exhibiting maximal activity. Though PGH contains steroids alone but

still it exhibited better activity than AGH because steroids were proved

to be involved in neuromodulatory effects [125]. In addition to

steroids, flavonoids were also present in CGH which might be

229

responsible for more activity of CGH than PGH and AGH. This may be

because of involvement of flavonoids and sterols in central inhibitory

and neuromodulatory effects [126]. Ethanol is a universal sovent

which extracts almost all the phytoconstituents. Our preliminary

phytochemical studies on EGH showed the presence of steroids,

flavonoids, alkaloids and tannins. Many flavonoids are reported to act

as benzodiazepine-like molecules in the central nervous system and

modulate GABA-generated chloride currents in animal models of

anxiety, sedation and convulsion [186-188], so they might be

responsible for the maximal activity of EGH.

Present study demonstrated that the ethanol extract showed

maximum activity in all three tested models. Out of three models,

ethanol extract exhibited more efficient protection against PTZ-

induced convulsions because EGH might increase the seizure

threshold and antagonize the action of PTZ. Further the presence of

flavanoids may partially contribute the significant activity of ethanol

extract of leaves of Gossypium herbaceum. Present study evidences

that plants rich in antioxidant principles can be used in the treatment

of epilepsy.

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