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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.

Protective Effects of &lt;i&gt;α&lt;/i&gt;-Tocopherol against Brain Tissue Damage Induced by Intracerebral Hemorrhage in SD Rats

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