脑缺血再灌注糖尿病大鼠海马CA1区凋亡基因的表达

Expression of apoptosis-related genes in focal cerebral ischemia-reperfusion injury in rats with diabetes mellitus

目的观察凋亡基因Bcl-2、Bax在糖尿病大鼠脑缺血再灌注海马CA1区神经元损伤中的表达。方法采用链脲佐菌素(STZ)诱导和线栓法制备糖尿病大脑中动脉闭塞模型(MCAO),应用HE染色和免疫组化方法比较糖尿病脑缺血再灌注组与缺血再灌注组海马CA1区神经元缺失、凋亡基因Bcl-2、Bax的表达。结果糖尿病脑缺血再灌注组海马CA1区神经元缺失,明显高于缺血再灌注组(P<0.05);缺血再灌注组及糖尿病脑缺血再灌注组大鼠海马CA1区Bcl-2、Bax阳性染色阳性细胞与正常对照组及假手术组比增多,差异显著(P<0.05),而糖尿病脑缺血再灌注组比缺血再灌注组增加得更明显,差异有显著性(P<0.05),其中Bax上调幅度大。结论糖尿病大鼠脑缺血再灌注损伤后海马CA1区细胞发生凋亡,Bcl-2、Bax介导的细胞凋亡机制可能是糖尿病加重脑缺血再灌注海马神经元损伤机制之一。

Objective To investigate the expressional sigrtificance of Bcl-2, Bax in hippocampus in focal cerebral ischemia-reperfusion injury（CIR I） in rats with diabetes mellitus.Methods By using streptozocin （STZ） and line-lock method to set up diabetes- MCAO model, immunohistochemieal and HE technique were used to examine the neuron death and expression of Fas protein after focal cerebral isehemia-reperfusion injury in rats with diabetes mellitus. Results Neuron death and up-regulation of Bcl-2, Bax were seen, which was more statistically significant in diabetes-MCAO group than that in cerebral reperfusion group（ P 〈 0.05）. Conclusion The cell apoptosis mediated by Bcl-2,Bax may be one of the mechanism that hippoeampus neuron injury in the focal cerebral ischemiareperfusion rats was aggravated by diabetes mellitus.