|Year : 2016 | Volume
| Issue : 2 | Page : 94-97
Anticonvulsant effect of Portulaca oleracea in experimental animal models
Mayanglambam Medhabati Devi, Leisangthem Tarinita Devi, Nameirakpam Meena Devi, Khomdram Krishna Pramodini Devi, Akham Subhalakshmi Devi
Department of Pharmacology, Regional Institute of Medical Sciences, Imphal, Manipur, India
|Date of Web Publication||24-May-2016|
Mayanglambam Medhabati Devi
Department of Pharmacology, Regional Institute of Medical Sciences, Lamphel, Imphal - 795 001, Manipur
Source of Support: None, Conflict of Interest: None
Background: Portulaca oleracea, locally known as Leipak-kundo, which belongs to portulacaceae family is an annual succulent prostrate herb with 15-30 cm long stem, fleshy leaves, and flowers. The plant is used for the treatment of gonorrhea, gum and teeth complaints, scurvy and liver diseases. The constituents of the plant are flavonoids, alkaloids, omega-3 fatty acid, and antioxidants. P. oleracea has been reported to possess hypoglycemic, anti-ulcer, muscle relaxant, analgesic, and anti-inflammatory properties. Materials and Methods: The anticonvulsant effect of the aqueous extract of P. oleracea leaves (200, 400, and 600 mg/kg, p.o.) was studied against seizures induced by maximal electroshock (MES) and pentylentetrazol (PTZ) in albino mice. Results: The aqueous extract of P. oleracea leaves decreased the duration of hind limb tonic extension phase and recovery time in MES model. It also decreased the time of onset and duration of clonic convulsion induced by PTZ. The aqueous extract of P. oleracea leaves exhibited significant anticonvulsant effect against MES and PTZ-induced seizures. Conclusion: The aqueous extract of P. oleracea leaves (200, 400, and 600 mg/kg) produced significant anticonvulsant effect against MES and PTZ-induced seizures in mice. The aqueous extract of P. oleracea may be potentiating the GABAergic transmission in the central nervous system.
Keywords: Anticonvulsant, maximal electroshock, pentylentetrazol, Portulaca oleracea, seizure
|How to cite this article:|
Devi MM, Devi LT, Devi NM, Pramodini Devi KK, Devi AS. Anticonvulsant effect of Portulaca oleracea in experimental animal models. J Med Soc 2016;30:94-7
|How to cite this URL:|
Devi MM, Devi LT, Devi NM, Pramodini Devi KK, Devi AS. Anticonvulsant effect of Portulaca oleracea in experimental animal models. J Med Soc [serial online] 2016 [cited 2021 Apr 12];30:94-7. Available from: https://www.jmedsoc.org/text.asp?2016/30/2/94/182908
| Introduction|| |
Epilepsy is one of the most common disorders of the central nervous system (CNS) with a prevalence of approximately 1% of the total population world over.  It is characterized by recurrent episodes of seizures with or without convulsion. The underlying abnormality of epilepsy is poorly understood, but it may be associated with an imbalance between excitatory and inhibitory neurotransmitters in the brain.  Despite the availability of over 25 anti-epileptic drugs, nearly 20% of people with epilepsy, especially those of partial epilepsy have intractable seizures that do not respond to even the best available treatment.  The currently available anticonvulsant suffers from drawbacks such as teratogenic and other dose-related side-effects. The ancient system of medicines provides a wide range of options for these problems with a vast source of medicinal plants, which are devoid of undesirable effects and are gaining popularity in most of the developing countries. 
Portulaca oleracea (Manipuri - Leipak-kundo; English - Common Purslane) which belongs to portulacaceae family is an annual succulent prostrate herb with 15-30 cm long stem, fleshy leaves, and flowers. It is grown abundantly all over india. The plant has been used for the treatment of gonorrhea, gum and teeth complaints, scurvy and liver diseases. ,,] The constituents of the plant are flavonoids,  alkaloids,  omega-3 fatty acid, and antioxidants.  P. oleracea has been reported to possess hypoglycemic,  anti-ulcer,  muscle relaxant,  analgesic and anti-inflammatory  and hepatoprotective  properties. However, no scientific study is available on neuropharmacological activities of P. oleracea. Therefore, this study was undertaken to investigate the anticonvulsant effect of P. oleracea against maximal electroshock (MES) and pentylentetrazol (PTZ) induced seizures in mice.
| MaterialS and methods|| |
Preparation of the extract
Fresh aerial parts of p. oleracea were collected from the campus of the Regional Institute of Medical Sciences, Imphal, identified and authenticated. The plant parts were cleaned, dried under shade. The leaves ware separated and powdered by a mechanical grinder. About 38 g of the pulverized leaves was extracted with distilled water using a Soxhlet apparatus.  The yield was 35.2%. The aqueous extract of P. oleracea leaves was administered after dissolving in distilled water to the animals.
Albino mice weighing 25-30 g were procured from the central animal house of the institute. They were housed in standard polypropylene cases and kept under room temperature with a 12 h light, dark cycle. The mice were given standard laboratory diet and water ad libitum. Food was withdrawn 8 h before and during experiments. All experimental protocols were approved by the Institutional Animal Ethics Committee (protocol approval number No. MU/6-5/MD-MS (Vol.1)/911).
PTZ (Sigma, USA), Phenytoin Sodium (Knoll Pharma, India), Sodium Valproate (Sun Pharma, India) were used in this study. The drugs were dissolved in distilled water and administered in a volume of 25 ml/kg.
Acute toxicity study
The aqueous extract of p. oleracea was administered in doses of 400, 800, 1600 and 3000 mg/kg, p.o. to four groups of mice, each consisting of ten mice and mortality was observed after 24 h. The aqueous extract of p. oleracea contains the active chemical constituents such as flavonoids  and antioxidants. 
Assessment of anticonvulsant effect
Maximal electroshock-induced seizures
All mice were pretested and those which did not show hind limb tonic extension (HLTE) were rejected.  The animals were divided into five groups. Each group consisted of six animals. The drug treatment schedule of the different groups is given in [Table 1].
|Table 1: Drug treatment schedule of the different groups (maximal electroshock - Induced seizures)|
Click here to view
All the drugs were administered orally 60 min before induction of seizures. Then seizures were induced by electroconvulsiometer (techno, India). A current of 50 mA was delivered transauricularly for a period of 0.2 s. via small alligator clips attached to each pinna. This current intensity elicited complete tonic hindlimb extension in control mice. To evaluate the drug effect on the seizure severity, the duration of tonic hind limb extension and recovery time were recorded.
Pentylenetetrazol induced seizures
The animals were divided into five groups.  Each group consisted of six animals. The drug treatment schedule of the different groups is given [Table 2].
|Table 2: Drug treatment schedule of the different groups (pentylentetrazol - Induced seizures)|
Click here to view
Seizures were induced by injecting PTZ (60 mg/kg) subcutaneously in the loose skin behind the neck of the mice 60 min following administration of drugs. The animals were observed for the onset and duration of clonic convulsion up to 30 min after PTZ challenge.
The result was analyzed for statistical significance using one-way ANOVA followed by Dunnett's t-test. P < 0.05 was considered significant.
| ResultS|| |
Anticonvulsant effects of aqueous extract of P. oleracea on MES and PTZ induced seizure in mice are shown in [Table 3] and [Table 4], respectively. It is evident from the [Table 3] that the standard drug (phenytoin sodium 20 mg/kg) produced full protection against MES-induced seizures indicated by the complete absence of tonic hind limb extension. The mean duration of tonic hind limb extension of the control group was 14 ± 0.56 s. The mean duration of hindlimb extension in the groups treated with the test drug at doses of 200, 400 and 600 mg/kg, p.o were 11.75 ± 5, 10.9 ± 1.0, and 9.25 ± 0.85, respectively. The test drug produced a significant decrease in the duration in hind limb extension phase when compared to control. The maximum decrease was observed with the dose of 600 mg/kg of the test drug. The total mean recovery time of the animals in the groups treated with test drug at doses of 200, 400 and 600 mg/kg were 45.5 ± 1.47 (P < 0.001), 37.1 ± 1.82 (P < 0.001), 29.7 ± 1.17 (P < 0.001) seconds, respectively. The mean recovery time in the control group was 58.5 ± 1.52 s.
|Table 3: Effects of aqueous extract of Portulaca oleracea on maximal electroshock induced seizure in mice|
Click here to view
|Table 4: Effects of aqueous extract of Portulaca oleracea on pentylentetrazol induced seizure in mice|
Click here to view
The onset and duration of clonic phase after PTZ induced seizure was observed in the albino mice. [Table 4] shows that the standard drug (sodium valproate 200 mg/kg) produced full protection against PTZ-induced seizure which was indicated by the complete absence of clonic convulsions. In the control group, it was observed that clonic convulsions appeared at 148.3 ± 8.36 s after PTZ and lasts for 11.5 ± 0.43 s. The mean onset of clonic convulsions in the test groups at doses of 200, 400, and 600 mg/kg were 190 ± 3.66 (P < 0.01), 315 ± 10.9 (P < 0.001), and 531.6 ± 18.03 (P < 0.001) sec, respectively. The duration of clonic phase after PTZ-induced seizure in the control group was 11.5 ± 0.43 s. The duration of clonic phase among the groups treated with test drug at doses of 200, 400 and 600 mg/kg were 6.05 ± 0.31 (P < 0.001), 4.16 ± 0.29 (P < 0.001) and 2.8 ± 0.21(P < 0.001) seconds, respectively. The extract significantly delayed the onset and reduced the duration of clonic convulsion phase. Thus, this study shows that the aqueous extract of P. oleracea in doses of 200, 400, and 600 mg/kg, p.o. exhibited a significant protection against MES and PTZ-induced seizure.
| Discussion|| |
Research into epilepsy and development of anti-epileptic drugs relies on studies in experimental animals. MES and PTZ-induced seizures are the mainstay of any anti-epileptic drug screening protocols. In this study, the anticonvulsant activity of P. oleracea was evaluated by MES and PTZ-induced seizure tests in albino mice. The MES is probably the best-validated method for assessment of anti-epileptic drugs in generalized tonic-clonic seizures.  MES causes several changes at the cellular level, which can disrupt the signal transduction in the neurons. One of the most important mechanism by which it causes cellular damage is the facilitation of Ca 2+ entry into the cell in a large amount and thus, prolonging the duration of convulsion.  Apart from Ca 2+ ions, MES also facilitates the entry of other positive ions such as Na + , blockade of which can prevent the MES-induced tonic extension. , Currently available anticonvulsant drugs such as valproate and phenytoin act by modulation of these ions channels.  On the other hand, potentiation of gamma-aminobutyric acid (GABA) receptors is also reported to protect against MES-induced seizures. The aqueous extract of P. oleracea was found to possess significant anticonvulsant activity in albino mice at doses of 200, 400, and 600 mg/kg, p.o against MES-induced seizure. The duration of HLTE of the control group (14 ± 0.56 s) was consistent with the finding of Manocha et al.  (15.34 ± 0.93 s). P. oleracea at doses of 200, 400 and 600 mg/kg, p.o was significant (P < 0.05-0.001) as compared to the control.
The PTZ-induced seizures are similar to the symptoms observed in absence seizures and anti-absence seizure drugs suppressed PTZ-induced seizures.  GABA is a major inhibitory neurotransmitter of CNS and increase in its level in the brain produces a variety of CNS-dependent effects including depression and anticonvulsant effect.  PTZ may be exerting its convulsive effect by inhibiting the activity of GABA at GABA A receptors, the major inhibitory neurotransmitter which is implicated in epilepsy.  The mean value of the time of onset of clonic convulsions (sec) of the control group was 148.3 ± 8.36 which was slightly more than the findings of Sonavane et al.  (110.0 ± 14.8). The aqueous extract of P. oleracea increased the time of onset of seizure after PTZ administration. Thus, investigation of aqueous extract of P. oleracea showed significant anticonvulsant activity against MES- and PTZ-induced seizures. The probable mechanism of anticonvulsant activity of the extract might be due to potentiation of GABAergic neurotransmission.
The phytochemical study of P. oleracea showed the presence of flavonoids, alkaloids, and antioxidants. These constituents are reported to have potent anticonvulsant effect in various seizure models.  Therefore, the presence of such compounds in the extract may be responsible for the anticonvulsant effect. Further research is required to elucidate its specific mechanism of action and responsible, active principles.
| Conclusion|| |
The aqueous extract of P. oleracea leaves (200, 400 and 600 mg/kg) produced significant anticonvulsant effect against MES and PTZ induced seizures in mice. The probable mechanism of anticonvulsant activity of the extract might be due to potentiation of GABAergic neurotransmission.
Financial support and sponsorship
Conflicts of interest
There are no conflicts of interest.
| References|| |
Delgado-Escueta AV, Treiman DM, Walsh GO. The treatable epilepsies. N Engl J Med 1983;308:1508-14.
Rang HP, Dale MM, Ritter JM, Flower RJ. Antiepileptic Drugs, Pharmacology. 7 th
ed. New Delhi: Churchill Livingstone Elsevier; 2012. p. 540-52.
Mattson RH. Drug treatment of partial epilepsy. Adv Neurol 1992;57:643-50.
Hedge K, Thakker SP, Joshi AB, Shastry CS, Chandrashekhar KS. Anticonvulsant activity of Carissa carandas
Linn. Root extract in experimental mice. Trop J Pharm Res 2009;8:117-25.
Chopra RN, Nayar SL, Chopra IC. Portulacaceae. Glossary of Indian Medicinal Plants. New Delhi: Council of Scientific and Industrial Research; 1956. p. 202.
Kiritikar KR, Basu BD. Portulaca
Linn. In: Blatter E, Caius JF, Mahaskar SK, editors. Indian Medicinal Plant. 2 nd
ed. Dehradun: International Book Distributors; 1987. p. 242-3.
Sinha SC, editor. Medicinal Plant of Manipur. 1 st
ed. Imphal: Manipur Association for Science and Society; 1996.
Xu X, Yu L, Chen G. Determination of flavonoids in Portulaca oleracea
L. by capillary electrophoresis with electrochemical detection. J Pharm Biomed Anal 2006 3;41:493-9.
Xiang L, Xing D, Wang W, Wang R, Ding Y, Du L. Alkaloids from Portulaca oleracea
L. Phytochemistry 2005;66:2595-601.
Simopoulos AP, Norman HA, Gillaspy JE, Duke JA. Common purslane: A source of omega-3 fatty acids and antioxidants. J Am Coll Nutr 1992;11:374-82.
Sinha BP, Varma SD. Hypoglycemic action of Portulaca
homogenates. Hoppe Seylers Z Physiol Chem 1962;327:274-5.
Karimi G, Hosseinzadeh H, Ettehad N. Evaluation of the gastric antiulcerogenic effects of Portulaca oleracea
L. extracts in mice. Phytother Res 2004;18:484-7.
Okwuasaba F, Ejike C, Parry O. Comparison of the skeletal muscle relaxant properties of Portulaca oleracea
extracts with dantrolene sodium and methoxyverapamil. J Ethnopharmacol 1987;20:85-106.
Chan K, Islam MW, Kamil M, Radhakrishnan R, Zakaria MN, Habibullah M, et al.
The analgesic and anti-inflammatory effects of Portulaca oleracea
L. subsp. Sativa
(Haw.) Celak. J Ethnopharmacol 2000;73:445-51.
Ahmad M, Itoo A, Baba I, Jain SM, Saxena RC. Hepatoprotective activity of P. oleracea
Linn. On experimental animal model. Int J Pharm Pharm Sci 2013;5:267-9.
Khosla P, Bhanwara S, Singh J, Srivastava RK. Antinociceptive activity of Azadirachta indica
(neem) in rats. Indian J Pharmcol 2000;32:372-4.
Swinyard EA, Brown WC, Goodman LS. Comparative assays of antiepileptic drugs in mice and rats. J Pharmacol Exp Ther 1952;106:319-30.
Desmedt LK, Niemegeers CJ, Lewi PJ, Janssen PA. Antagonism of maximal metrazol seizures in rats and its relevance to an experimental classification of antiepileptic drugs. Arzneimittelforschung 1976;26:1592-603.
Löscher W, Fassbender CP, Nolting B. The role of technical, biological and pharmacological factors in the laboratory evaluation of anticonvulsant drugs. II. Maximal electroshock seizure models. Epilepsy Res 1991;8:79-94.
Inan S, Büyükafsar K. Antiepileptic effects of two Rho-kinase inhibitors, Y-27632 and fasudil, in mice. Br J Pharmacol 2008;155:44-51.
Bum EN, Nkantchoua GN, Njikam N, Taiwe GS, Ngoupaye GT, Pelanken MM. Anticonvulsant and sedative activity of leaves Senna spectabilis
in mice. Int J Pharmacol 2010;6:123-8.
Manocha A, Sharma KK, Medirata PK. Anti-convulsant effect of nalbuphine on maximal electroshock seizure in mice. Indian J Pharmacol 1998;30:306-10.
Mc Namara JO. Drug effective in the treatment of epilepsies In. Burton LL, Lazo JS, Parker KL, editors. Goodman and Gillman′s the Pharmacological Basis of the Therapeutics. 12 th
ed. New York: McGraw-Hill; 2011. p. 583-607.
Macdonald RL, McLean MJ. Cellular bases of barbiturate and phenytoin anticonvulsant drug action. Epilepsia 1982;23 Suppl 1:S7-18.
Pritchard TC, Aloway KD. Medical Neurosciences. USA, Rochester: Mayo Foundation; 1994. p. 307-12.
Sonavane GS, Palekar RC, Kasture VS, Kasture SB. Anticonvulsant and behavioural actions of Myristica fragrans.
Indian J Pharmacol 2002;34:332-8.
[Table 1], [Table 2], [Table 3], [Table 4]