脑缺血过程中B细胞淋巴瘤-2基因家族基因的表达及与细胞死亡的关系

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

THE EXPRESSION OF bcl 2 FAMILY GENES AND RELATIONSHIP WITH CELL DEATH DURING ISCHEMIA

In order to recognize the patterns of the expression of bcl 2 family genes and their effect in regulating neuron death after ischemia, The model of global ischemia was made by occluding bilateral common carotid and vertebral arteries in this study. The expression of Bax, bcl xL, and bcl 2 genes and relations between the expression of bcl 2 family gene and apoptosis were observed. The immunostaining for Bax increased at 6h during ischemia reperfustion. The peak was appeared in 24 48h. The expression of Bcl xL mRNA decreased at 24h after the onset of reperfusion. The immunostaining for bcl xL was markedly decreased at 48h after ischemia. The change of Bax and bcl xL expression was more significant in sensitive neurons to ischemia. In contrast to Bax and bcl xL, the significant changes of bcl 2 mRNA and protein expression were not detected. The findings suggest that Bax, bcl xL may contribute to regulation of neuron death during ischemia reperfustion. There might be significant relationship between the changes of the expression of bcl xL and Bax genes and neuronal sensitivity to ischemia.