Cerebroprotective effect of Eclipta alba against global model of cerebral ischemia induced oxidative stress in rats

Oxidative stress is believed to contribute to neuronal damage induced by cerebral ischemia/reperfusion (I/R) injury. The present study was undertaken to evaluate the possible cerebroprotective and antioxidant effect of hydroalcoholic extract of Eclipta alba against global cerebral ischemia in the rat. Adult Wistar albino rats were treated with extract of Eclipta alba (250 and 500 mg/kg/day, p.o.) for 10 days. The global cerebral ischemia-reperfusion injury was induced by occluding bilateral common carotid arteries (BCCA) for 30 min, followed by 4 h reperfusion. Quercetin (20 mg/kg, i.p.) was used for the reference compound. After that, animals were sacrificed by decapitation, brain was removed, various biochemical estimations, cerebral edema, assessment of cerebral infarct size, and histopathological examinations were carried out. BCCA caused significant depletion in superoxide dismutase (SOD), glutathione peroxidase (GPx), reduced glutathione (GSH), catalase (CAT), glutahione-S-transferase (GST), glutathione ruductase (GR) and significant increase in malondialdehyde (MDA) in brain. Pretreatment with hydroalcoholic extract of Eclipta alba significantly reversed the levels of biochemical parameters and significantly reduced the edema and cerebral infarct size as compared to the ischemic control group. Eclipta alba at higher dose markedly reduced ischemia-induced neuronal loss of the brain. Reduction of cerebral edema, an early symptom of ischemia, is one of the most important remedies for reducing subsequent chronic neural damage in stroke. The results of the study show that Eclipta alba pretreatment ameliorates cerebral ischemia/reperfusion injury and enhances the antioxidant defense against BCCA occlusion induced I/R in rats: so it exhibits cerebroprotective property. HPLC fingerprint of hydroalcoholic extract of Eclipta alba was performed for conforming the coumestan present in the plant extract. (C) 2012 Elsevier GmbH. All rights reserved.