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目的 探讨大鼠脑缺血再灌注时蛋白激酶 C(PKC)活性的变化与 FOS、BCL- 2表达的关系。方法 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天时仍有少量表达。 BCL - 2表达的高峰是在缺血再灌注 2天时。结论 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
Objective To investigate the relationship between the changes of protein kinase C (PKC) activity and the expressions of FOS and BCL-2 during cerebral ischemia-reperfusion in rats. Methods Rat middle cerebral artery occlusion (MCAO) model was established. The activity of PKC was detected by phosphoryl transfer and the contents of BCL-2 and FOS were detected by immunohistochemistry. Results The activity of PKC increased continuously after ischemia-reperfusion, FOS increased obviously in the early stage of ischemia-reperfusion, and remained low till the 2nd day after ischemia-reperfusion. The peak of BCL - 2 expression was at 2 days after ischemia - reperfusion. Conclusion PKC translocates during ischemia-reperfusion, and PKC promotes the expression of FOS and BCL-2. The combination of these factors may affect the apoptosis of nerve cells