Naringenin attenuates cerebral Ischemia-Reperfusion injury through Inhibiting oxidative stress and Inflammation in Diabetic Rats

Aim: Ischemic stroke is one of the important complications of diabetes. Diabetes exacerbate cerebral injury after ischemia and reperfusion. This study was designed to investigate whether the naringenin has a cerebroprotective action against the ischemic reperfusion injury via anti-oxidant and anti-inflammatory mechanisms in diabetic rats. Diabetes was induced by Streptozocine (50mg/kg) intraperitoneal injection at once. Medial carotid artery occlusion (30 min) and reperfusion (3 hr) was employed to induce cerebral infarction in diabetic rats. The animals were divided in to groups as: normal, sham, ischemia-reperfusion and naringenin treated (50, 100, 150 and 200mg/kg). These were used for evaluation of percentage of cerebral infarction. Further, 200mg/kg dose was selected for the estimation of inflammatory biomarkers such as Tumor necrosis factor-α, Interlukin-6, Interlukin-10 and oxidative stress biomarkers such as malondialdehyde, superoxide dismutase, and catalase were estimated and histopathological changes were studied. Dose dependent reduction in percentage of cerebral infarction was observed in narigenin treated groups. With Naringenin 200mg/kg dose, inflammatory and oxidative stress markers like Tumor necrosis factor-α, Interlukin-6, myeloperoxidase and malondialdehyde levels were distinctively reduced and there was a remarkable increased levels of anti-inflammatory and anti-oxidant markers like Interlukin-10, catalase, and superoxide dismutase. Conclusion: Collectively, these findings demonstrate that the mechanism (s) responsible for a cerebroprotective effect of naringenin against the ischemic reperfusion injury in the diabetic rats involves anti-oxidant and anti-inflammatory actions.