大鼠脑缺血再灌注与蛋白激酶C活性变化及FOS、BCL-2的表达

目的 探讨大鼠脑缺血再灌注对时蛋白激酶Ｃ（ＰＫＣ）活必珠变化与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，用免疫组化检测ＢＣＬ－２及ＦＯＳ的量。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

PKC activity,FOS and BCL-2 expression after cerebral ischemia-reperfusion in rats

Objective To research the relationship between the change of protein kinase C(PKC) activity and the expression of FOS, BCL 2 during cerebral ischemia reperfusion.Methods Middle cerebral artery ischemia reperfusion model was established in Wistar rats. In these regions the changes of PKC activity were measured by phosphoryl transfer pieces. The contents of BCL 2 and FOS were observed with immunohistochemistry.Results The PKC activity in membrane increased continuously after cerebral ischemia reperfusion.FOS increased remarkably at early stage of reperfusion,there was a small amount expression till 2 d of reperfusion. The peak of BCL 2 expression was at reperfusion 2 d.Conclusion PKC took place translocation activation during cerebral ischemia reperfusion,PKC promoted the expression of FOS and BCL 2. Their complex role influenced the neuronal apoptosis