摘要
目的 探讨蛋白激酶C(PKC)与神经元凋亡的可能机制。方法 采用大鼠全脑缺血模型 ,观察脑缺血 再灌流后PKC活性、FOS表达及神经元凋亡的变化。结果 脑缺血 再灌流可以导致PKC的移位激活伴FOS表达及神经元凋亡的增加 ;用蛋白激酶C抑制剂灯盏花可以阻止上述变化。结论 蛋白激酶C的激活可能通过促进FOS表达参与了脑缺血
Objective To explore the possible mechanism by which protein kinase C (PKC) involves in the neuronal apoptosis induced by cerebral ischemia/reperfusion Methods After the model of ischemia/reperfusion was established in male Wistar rats, PKC activity, FOS protein expression and neuronal apoptosis in their brains were observed The effect of PKC inhibitor, Dengzhanghua, on above indexes were studied at the same time Results Cerebral ischemia/reperfusion resulted in transloactional activation of PKC, accompanied with the increase of FOS expression and neuronal apoptosis Dengzhanghua prevented against the above changes Conclusion Activated PKC is involved in ischemia/reperfusion induced neuronal apoptosis by regulating FOS expression
出处
《第三军医大学学报》
CAS
CSCD
北大核心
2002年第12期1385-1387,共3页
Journal of Third Military Medical University
基金
国家自然科学基金资助项目 ( 396 70 2 6 9)