摘要
目的:探讨蛋白激酶C激活参与神经元凋亡的可能机理。方法:采用大鼠全脑缺血模型,观察脑缺血/再灌流后蛋白激酶C活性、Bcl-2表达及神经元凋亡的变化。结果:脑缺血/再灌流可以导致蛋白激酶C的移位激活伴Bcl-2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的激活促进Bcl-2表达可能与脑缺血/再灌流诱导的神经元凋亡有关。
Objective To explore the mechanism of protein kinase C (PKC) involved in neuronal apoptosis induced by cerebral ischemia/reperfusion. Methods After the model of ischemia/reperfusion was established in male Wislar rats, the changes in PKC activity, Bcl-2 protein expression and neuronal apoptosis were determined. The effect of PKC inhibitor (Denyzhanghua injection) on PKC activity,Bcl-2 protein expression and neuronal apoptosis was observed. Result The cerebral ischemia/reperfusion could result in PKC translocational activation accompanied with the increases in the experssion of Bcl-2 protein and neuronal apoptosis. Denyzhanghua could prevent the above-mentioned changes. Conclusion The increase in the expression of Bcl-2 produced by activated PKC may be related to the neuronal apoplosis induced by the cerebral ischemia/reperfusion.
出处
《华南国防医学杂志》
CAS
2004年第4期25-28,共4页
Military Medical Journal of South China
基金
国家自然科学基金项目(编号39670269)