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探讨脑缺血再灌注时 PKC活性的变化与 FOS、BCl- 2表达的关系 ,采用大鼠大脑中动脉缺血再灌注模型 ,用磷基转移片检测 PKC的活性 ,用免疫组化法检测 BCl- 2及 FOS的含量。结果 :缺血再灌注后膜 PKC活性持续增加。FOS在缺血再灌注早期即有明显增加 ,至缺血再灌注 2 d时仍有少量表达。BCl- 2表达的高峰是在缺血再灌注 2d时。提示 :缺血再灌注期间 PKC发生易位激活 ,PKC促进了 FOS和 BCl- 2的表达 ,这几个因素综合作用影响神经细胞凋亡。
To investigate the relationship between the changes of PKC activity and the expression of FOS and BCl-2 in cerebral ischemia-reperfusion rats. The model of middle cerebral artery occlusion (MCAO) in rats was established. The activity of PKC was detected by phospho- - 2 and FOS content. Results: The membrane PKC activity increased continuously after ischemia-reperfusion. FOS significantly increased in the early stage of ischemia-reperfusion, and still a small amount of expression 2 d after ischemia-reperfusion. The peak of BCl-2 expression was at 2 days after ischemia-reperfusion. Tip: PKC during ischemia-reperfusion translocation activation, PKC promote FOS and BCl-2 expression, a combination of these several factors affect neuronal apoptosis.