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Anticonvulsant effect of Boswellia serrata by modulation of endogenous biomarkers | Abstract
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Abstract

Anticonvulsant effect of Boswellia serrata by modulation of endogenous biomarkers

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

Epilepsy is a group of disorders of CNS bearing its pathological origin in paroxysysmal cerebral dysrhythmia, clinically consisting episodes (seizure) of loss of consciousness. Boswellia serrata is a tetrahydroxy flavone that possess antiyperlipidemic, antioxidant, anti-inflammatory and antidiabetic potential. The aim of present investigation was to investigate the anticonvulsant activity of Boswellia serrata (5, 10 and 200 mg/kg) against Pentylenetetrazole (PTZ), Strychnine (STR), Isoniazid (INH) and maximal electroshock (MES) induced convulsions in mice as well as Electrical kindling seizures in rats. Diazepam and Phenytoin were used as reference anticonvulsant drugs for comparison. Intraperitoneal administration of PTZ (90mg/kg), Strychnine (50 mg/kg) and Isoniazid (300 mg/kg) resulted in hind-limb, tonic-clonic convulsion along with lethality in mice, whereas twice daily auricular stimulation resulted progressive severity of seizures in rats. 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 Boswellia serrata (10 and 200 mg/kg) delayed onset of convulsion along with duration of tonicclonic convulsions as well as it significantly reduced PTZ and STR-induced mortality in mice (P < 0.05 - P < 0.001). It also significantly (P < 0.001) reduced severity of electrically kindled seizures in rats and total number of rats seizure per group. Mice treated with Boswellia serrata (10 and 200 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 Boswellia serrata. 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.