Protective Effects of α-Tocopherol against Brain Tissue Damage Induced by Intracerebral Hemorrhage in SD Rats

Lipid peroxidation mediated by oxygen radical is one of the main mechanisms underlying secondary brain injury. Among all vitamin E compounds, α-tocopherol shows the most prominent antioxidative effects. It plays an important role in cell aging and injury. However, there has been no report regarding the effects of α-tocopherol on changes in brain tissue morphology after intracerebral hemorrhage (ICH), cerebral edema, or the expression of Bax and Bcl-2 proteins. We use SD rats to carry out the related studies; based on the atlas of SD rats, the caudate nucleus was positioned using a stereotaxic apparatus, and 50 μl autologous tail artery blood was injected to caudate nucleus in the ICH and α-tocopherol groups to establish ICH model. Rats in the sham surgery group received the same volume of saline in the caudate nucleus. Rats in the α-tocopherol group received intraperitoneal injections of α-tocopherol at 600 mg/kg every day. Rats in the ICH group and sham surgery group received the same amount of saline at the same times as those in the α-tocopherol group. We observed some interesting results: comparisons of brain tissue sections of rats from different groups showed that brain tissue damage and functional neurological deficits among rats from the α-tocopherol group were less pronounced than in the ICH group. Wet weight/ dry weight measurement showed that rats from the α-tocopherol group exhibited less cerebral edema than those in the ICH group. Rats from the α-tocopherol group showed less Bax expression and more Bcl-2 expression than those in the ICH group.