Neuroprotective Role of Trolox in Hippocampus after Ischemia Reperfusion Injury in Mouse.

Cerebral ischemia is worldwide the third largest cause of mortality and disability in old people, and oxidative stress plays a considerable role in this process. In this study, for the fi rst time, we evaluated the effects of Trolox as an antioxidative agent in ischemia induced by reperfusion. Twenty-four Syrian male mice were randomly divided into the 3 groups. Both common carotid arteries of Syrian mice were ligated bilaterally for 20 min, blood fl ow was restored and Trolox (50 mg/kg) was immediately injected after induced ischemia. Shuttle box results showed an improvement in memory in the Trolox group compared to the ischemia group, however, these improvements were not signifi cant. Histopathological results showed a signifi cant increase in the number of healthy cells in the hippocampal CA1 region in the Trolox group compared to the ischemia group (p < 0.001). Also, caspase-3, as an apoptosis marker, was signifi cantly decreased in the Trolox group compared to the ischemia group (p < 0.01). Ultimately, as an anti-apoptotic factor, c-JUN was increased statistically in the Trolox group compared to the ischemia group (p < 0.01). Our study showed that after cerebral ischemia reperfusion, Trolox prescription increased anti-apoptotic proteins and decreased proapoptotic proteins thus protects neurons of the hippocampus and caused improvement of memory. Ultimately, these results would suggest some important treatment strategies after cerebral ischemia reperfusion.