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Animal care followed the official governmental guidelines in compliance with the CPCSEA, New Delhi and experimental protocols were conducted with the approval of the Ethics Committee of Andhra University, Visakhapatnam, India. Cerebral infarction was induced by Bi-lateral common carotid artery (BCA) occlusion method described by Iwasakhi et?al9 briefly; rats were anesthetized with thiopental sodium (30?mg/kg). Cervical vertebrae and the common carotid arteries were then exposed carefully separated from the vagus nerve. These arteries were occluded for 30?min followed by reperfusion for [http://www.selleckchem.com/products/Vandetanib.html Vandetanib] 4?h. The rectal temperature was maintained at 37?��?0.5?��C with a feedback-controlled heating-pad. Animals which did not lose the righting reflex or convulsed during the ischemic episode were excluded. Aqueous root extract of coleus edulis was administered by 15 days pre-treatment at doses of 150, 250 and 300?mg/kg orally. Rats were randomly divided into groups: Sham control, I/R control (Ischemia/reperfusion) and I/R?+?ACE (3 doses). Each group contains 6 animals. After predetermined time point of ischemia/reperfusion, the brains were quickly removed and sliced into coronal sections of 2?mm thickness. Each slice was immersed in a 1.0% solution of 2,3,5-triphenyltetrazolium chloride (TTC) for 30?min. Necrotic infarcted tissue was unstained and viable tissue [http://en.wikipedia.org/wiki/Oxalosuccinic_acid Oxalosuccinic acid] was stained dark red, further separated and weighed. Percentage of infarction was calculated.10 In selected group of animals were pre treated with 250?mg/kg po dose, brain tissues were isolated and used for the estimation of malondialdehyde (MDA),11 superoxide dismutase (SOD),12 and catalase (CAT).13 Data has been represented as mean?��?SEM and analyzed by one-way analysis of variance (ANOVA) followed by Tukeys t test (P?[http://www.selleckchem.com/products/Bosutinib.html Bosutinib ic50] compared to sham control group. A significant dose dependent reduction in percent cerebral infarction was observed with ACE administration. Results were shown in Table 1. MDA levels were significantly increased and SOD, CAT levels were significantly decreased in I/R of rats as compared to sham control group. In ACE treated groups, MDA levels were significantly reduced and SOD and CAT levels were increased significantly. Results were shown in Table 2. After BCA occlusion and reperfusion, several pathological events occur, oxidative stress is one of the most important events to worsen the ischemic condition. Earlier reports suggested that, further increased oxidative stress leads to tissue apoptosis.14?and?7 Free radicals were generated during ischemia and cause oxidative stress and alter the anti oxidative defenses in biological system. All the cells and tissues are equipped with anti oxidative enzymes like superoxide dismutase (SOD), glutathione peroxidase (GPX), glutathione reductase (GRD) and substances like reduced glutathione (GSH).