缺血脑组织中Bax和Bcl-2的表达在缺血性脑损伤发生中的作用

Expression of Bax and Bcl-2 in brain tissue for the occurrence of is hcemic brain damage

目的:检测脑梗死后Bax,Bcl-2在脑组织中的表达情况,探讨脑梗死的机制。方法:用线栓法制成Wistar大鼠大脑中动脉永久性闭塞模型(大脑中动脉脑梗死),精心饲养7d后断头取脑,用免疫组织化学方法检测各脑区Bax和Bcl-2的表达情况,并与正常组对照。结果:单侧脑梗死后,双侧大脑皮质、基底核、海马及齿状回表达Bcl-2和Bax的水平均增高(FBcl-2=270.796,P=0.000;FBax=543.042,P=0.000),不同部位双侧增高的程度不一致。其中,Bax的表达与Bcl-2的表达水平明显不等,梗死侧皮质Bax阳性细胞数为(14.65±0.41)个/视野,Bcl-2为(11.13±0.61)个/视野(t=18.240,P=0.000);海马Bax为(7.39±1.38)个/视野,Bcl-2为(5.78±1.64)个/视野(t=3.199,P=0.007);基底核Bax为(7.39±1.38)个/视野,Bcl-2为(4.09±0.29)个/视野(t=9.611,P=0.000),前者明显增高。结论:Bax的高表达可能是引起缺血性脑损伤的机制之一,而Bcl-2的表达增高可能起保护作用。均有差异,齿状回无差别。

AIM:To detect the expression of Bax and Bcl-2 in the brain tissue after cereb ral infarction(CI) in order to explore the CI mechanism. METHODS:Permanent models of middle cerebral artery occlusion(MCAO)by nylon sut ure embolization were made in rats.Seven days after operation, the rats were dec apitated and the brains were taken out.Immunohistochemical method was used to in vestigate the expressions of Bax and Bcl-2 in the CI group and normal control g roup for comparison. RESULTS:Higher levels of Bax and Bcl-2 expression were detected in cerebral c ortex, basal nuclei, hippocampus and dentate gyrus after unilateral CI,but the l evels of bilateral expressions were different in some region(FBcl-2=270.796,P =0.000;FBax=543.042,P=0.000).And the expression of Bax was significantly high er than that of Bcl-2 in the ischemic regions[crebral cortex:(14.65±0.41) vs(1 1.13±0.61)per visual field, t=18.240,P=0.000;hippocampus:(7.39±1.38) vs (5.78 ±1.64) per visual field,t=3.199,P=0.007;basal nuclei:(7.39±1.38) vs(4.09±0.29 ) per visual field,t=9.611,P=0.000]. CONCLUSION:High expression of Bax may be one of the mechanisms inducing brain damage,while high expression of Bcl-2 may play a protective role in brain damag e.