Assessment of oxidative stress status and neuroprotection by vitamin E in chronic cerebral hypoperfusion-induced neurodegeneration in rats

Background: A persistent reduction in regional cerebral blood flow (CBF) compromises memory and cognitive functions in the elderly leading to neurological illnesses. To unravel the neuropathological consequences of a reduced CBF, a similar condition has been created in rats by common carotid artery occlusion (2 vessel occlusion, 2VO). Oxidative stress, caused due to a disproportionate release of reactive oxygen species (ROS), has been associated with neuronal cell death in various regions of the brain. Objective: To study the antioxidant and neuroprotective effects of Vitamin E in chronic cerebral hypoperfusion induced neurodegeneration in rats. Methods: After acclimatization, twenty four Sprague Dawley rats weighing 200-250 g were equally divided into three groups. Group A – sham control, Group B–2VO, and Group C–2VO+E (treated daily with Vit E, 100 mg/kg, orally following 2VO). On the 8th week, all the rats were euthanized and the hippocampi were isolated. Viable neuronal cell count in the hippocampal CA-1 region was estimated. The Isoprostane F2 (Iso-F2) levels were also measured in the brain homogenates to quantify the oxidative stress levels Results: There was significant difference in neuronal cell death in 2VO group as compared to sham group. In 2VO+E rats, the viable neuronal cell count of the hippocampal CA-1 region was significantly higher (p<0.05) as compared to the 2VO group. Moreover, Iso-F2 levels in 2VO group was significantly higher (p