Bcl-2、Bax蛋白产物在脑缺血耐受中的表达及前列腺素E1的干预作用

目的探讨大鼠脑缺血时凋亡相关基因Bcl-2、Bax蛋白的表达与脑缺血耐受的关系及前列腺素E1 (PGE1)对脑缺血耐受的影响。方法采用大鼠全脑-局灶脑缺血耐受模型。观察预缺血组、PGE1组在大脑中动脉梗死2h再灌注(MCAO)24h后神经行为评分、脑梗死体积、Bcl-2、Bax蛋白表达和TUNEL、流式细胞仪检测神经细胞凋亡。结果MCAO后24h,PGE1组的神经行为评分、脑梗死体积、Bax蛋白表达更少,Bcl-2蛋白表达较高,神经细胞凋亡降低。结论预缺血及PGE1预处理后,使Bax蛋白表达减少,Bcl-2蛋白表达增高能够诱导脑缺血耐受,且PGE1的作用优于预缺血。

The expression of Bcl-2 and Bax and the influence to them of pros-taglandinE1 in cerebral ischemic tolerance

Objective To investigate the relationship between Bcl-2 and Bax expression in cerebral ischemia as well as the influence to cerebral ischemia tolerance of prostaglandin EI(PGE1).Methods Whole brain-local is- chemic tolerance model was used in the study.At 24h after MCAO,the neurophysical mark was recorded,the vol- ume of the cerebral infarction and the positive neurons of Bcl-2 and Bax were detected.Apoptosis rate of nerve cells by TUNEL and flow cytometry were studied.Results At 24h after MCAO,compared with brain ischemic precon- ditioning group,the neurophysical mark,the volume of the cerebral infarction and the Bax positive neurons of PGE1 group were lower,Bcl-2 positive neurons of PGE1 group were higher and the apoptosis rate of nerve cells of PGE1 group was decreased.Conclusions Both brain ischemic pre-conditioning and PGE1 could induce cerebral ischemic tolerance through increasing Bcl-2 expression and reducing Bax expression.The effect of PGE1 in inducing cerebral ischemic tolerance was better than that of brain ischemic pre- conditioning.