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为了了解Ｂ细胞淋巴瘤－２基因（ｂｃｌ－２）家族基因在脑缺血后表达规律及其调节细胞死亡的作用，通过阻塞大鼠双侧颈总动脉和椎动脉建立全脑缺血模型，观察了Ｂａｘ、ｂｃｌ－ｘＬ及ｂｃｌ－２基因表达变化以及与细胞死亡的关系。在缺血再灌流６ｈ，Ｂａｘ免疫染色增加，２４～４８ｈ达到高峰，ｂｃｌ－ｘＬｍＲＮＡ在２４ｈ后表达下降，ｂｃｌ－ｘＬ蛋白在４８ｈ可见明显降低，并且在缺血敏感神经元Ｂａｘ和ｂｃｌ－ｘＬ表达变化显著，与细胞凋亡发生的部位一致，相反，ｂｃｌ－２ｍＲＮＡ和蛋白表达未见明显变化。提示ｂｃｌ－ｘＬ和Ｂａｘ可能参与脑缺血再灌流中神经细胞死亡的调节，其表达变化与神经元对缺血的敏感性相关
In order to understand the expression of Bcl-2 gene after cerebral ischemia and its role in the regulation of cell death, a model of global cerebral ischemia was established by occluding bilateral common carotid arteries and vertebral arteries in rats. The changes of Bax, bcl-xL and bcl-2 gene expression and cell death were observed. The expression of bcl-xL mRNA decreased significantly after 24 h and the expression of bcl-xL protein decreased significantly at 48 h after ischemic reperfusion. The expression of Bax and bcl-xL in ischemic sensitive neurons increased Change significantly, and the site of apoptosis consistent, on the contrary, bcl-2mRNA and protein expression no significant change. These results suggest that bcl-xL and Bax may be involved in the regulation of neuronal cell death during cerebral ischemia and reperfusion, and their changes are related to the neuronal sensitivity to ischemia