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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 被引量:26

THE EXPRESSION OF bcl 2 FAMILY GENES AND RELATIONSHIP WITH CELL DEATH DURING ISCHEMIA
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摘要 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。 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.
出处 《解剖学报》 CAS CSCD 北大核心 1998年第2期119-123,I002,共5页 Acta Anatomica Sinica
关键词 脑缺血 细胞凋亡 BCL-2基因 BCL-XL基因 schemia Apoptosis bcl 2 bcl xL Bax Rat
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参考文献2

  • 1赵士福,国外医学.脑血管疾病分册,1996年,4卷,3期,169页
  • 2蔡文琴,实用免疫细胞化学与核酸分子杂交技术,1994年,406页

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