大鼠全脑缺血/再灌流脑组织蛋白激酶C活性的变化

Changes of activity of protein kinase C during cerebral ischemia/reperfusion in rats

目的：探讨脑缺血／再灌流致蛋白激酶Ｃ（ＰＫＣ）活性变化的规律及其参与神经元损伤的机制。方法：采用Ｗｉｓｔａｒ大鼠４血管闭塞模型，观察脑缺血／再灌流致ＰＫＣ活性（用磷基转移法测得ＰＫＣ活性）变化的规律，结合既往的研究讨论ＰＫＣ活性改变参与神经元损伤的机制。结果：脑缺血／再灌流可以致膜性ＰＫＣ活性明显增加，同时胞浆ＰＫＣ活性明显下降。结论：脑缺血／再灌流可以致ＰＫＣ移位激活。ＰＫＣ移位激活参与脑损伤的机制可能与其促进钙超载有关。

Objective: To explore the changes of activity of protein kinase C (PKC) during ischemia/reperfusion and the role of this enzyme in neuronal ischemic injury. Methods: After the model of ischemia/reperfusion was established in male Wistar rats, the changes of activity of PKC were observed. Results: Cerebral ischemia/reperfusion significantly increased the activity of membrane PKC and decreased that of cytosolic PKC. Conclusion: Cerebral ischemia/reperfusion results in translocational activation of PKC and the activation might damage the neurons through promoting calcium overload.