大鼠局灶性脑缺血预处理的抗细胞凋亡作用机制的研究

目的研究大鼠短暂局灶性脑缺血预处理对再次脑缺血神经细胞凋亡的保护作用,及bcl-2、bax与脑缺血耐受的关系.方法用开颅方法阻断大鼠大脑中动脉(MCA)20分钟,3天后再次阻断6小时.观察大鼠脑梗死体积及组织病理学改变,采用TUNEL法观察神经细胞凋亡状况,采用免疫组织化学方法观察bcl-2、bax蛋白表达的改变.结果与假预处理组和缺血组相比,预处理后缺血组梗死灶体积明显减小(均P＜0.01),半影区凋亡细胞数明显减少(P＜0.01),bax蛋白表达下降(P＜0.05),bcl-2蛋白表达显著上升(P＜0.01).结论 20分钟局灶性脑缺血预处理能够通过bcl-2表达增加及bax表达下降对再次脑缺血神经细胞起保护作用.

Study on anti-apoptosis effect of focal cerebral ischemic preconditioning in rAts

Objective To study the protective effect on transient focal cerebral ischemic preconditioning against neuronal cell apoptosis again,and the relationship between bcl 2, bax and cerebral ischemic tolerance.Methods Middle cerebral artery occlusion (MCAO) was showed for 20 min by craniotomy and MCA was blocked 6 h after 3 d.Cerebral infarct volume and the change of histopathological in rats were observed,the status of neuronal cell apoptosis were observed by TUNEL mothod,the alteration of bcl 2 and bax protein expression were observed by immunohistochemical method.Results As compared with the false preconditioning group and ischemia group,the infarct volume in the ischemic group reduced significantly after preconditioning( P < 0.01 ),the number of neuronal cell apoptosis reduced significantly in penumbra( P < 0.01 ),the expression of bax protein reduced( P < 0.05 ),the expression of bcl 2 protein increased significantly( P < 0.01 ).Conclusion 20min focal ischemic preconditioning could play a protective effect to cerebral ischemic neuronal cell apoptosis through the increasing of bcl 2 expression and the reduceion of bax expression.