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Anticonvulsant effect of Phylanthus amarus by modulation of endogenous biomarkers | Abstract
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Abstract

Anticonvulsant effect of Phylanthus amarus by modulation of endogenous biomarkers

Author(s): Ziyaurrahman A.R, Dr. Jayvadan Patel

Epilepsy is a neurological disorder that affects a wide range of people throughout the world. It is a disorder of brain characterize by unpredictable and periodic occurrence of a transient alteration of behavior due to the disordered, synchronous and rhythmic firing of populations of brain neurons. Incidence of epilepsy in developed countries is approximately 50 per 100,000 while that of developing country is 100 per 100,000 (WHO, 2006). It has been observed that the presently available antiepileptic drugs are unable to control seizures effectively in as many as 25% of the patients. The aim of present investigation was to evaluate the anticonvulsant activity of alcoholic extract of Phylanthus amarus (30, 60 and 120 mg/kg) against Pentylenetetrazole (PTZ), Picrotoxin (PTX) and maximal electroshock (M.E.S.) induced convulsions in mice. Diazepam and Phenytoin were used as reference anticonvulsant drugs for comparison. Intraperitoneal administration of PTZ (80mg/kg) and subcutaneous administration of picrotoxin (3.5 mg/kg) resulted in tonic-clonic convulsion along with lethality in mice. It also significantly altered levels of brain Gamma amino butyric acid (GABA) along with nitric oxide (NO) and xanthine oxidase (XO) in mice. Treatment with p. amarus (60 and 120 mg/kg) delayed onset of convulsion along with duration of tonic-clonic convulsions as well as it significantly reduced PTZ and PTXinduced mortality in mice (P < 0.05 - P < 0.001). Mice treated with P. amarus (120 mg/kg) significantly increased level of brain GABA whereas it significantly decreased elevated level of brain NO and XO. In conclusion, the findings of present study provide pharmacological credence to anticonvulsant profile of P. amarus. The protection against the convulsions and restoration of endogenous enzyme level give an innuendo to its probable mechanism of action which may be mediated through the GABAergic pathway and inhibition of oxidative injury.