摘要
目的 :探讨蛋白激酶C(ProteinkinaseC,PKC)参与神经损伤的机制。方法 :采用大鼠全脑缺血模型 ,观察脑缺血/再灌流后突触体游离钙的变化及PKC的抑制剂灯盏花对突触体游离钙的影响。结果 :脑缺血/再灌流可以导致突触体游离钙增加的抑制剂灯盏花可以阻止脑缺血/再灌流导致突触体游离钙增加。结论 :PKC参与神经元缺血性损伤可能与其促进钙内流有关。
Objective: To investigate the role of protein kinase C (PKC) in ischemic neuronal injury. Methods: After the model of ischemia/reperfusion was established in male Wistar rats, the changes of activity of PKC and intraneuronal free calcium content were observed. Meanwhile, the effects of Dengzhanhua, the PKC inhibitor, on the two parameters were also observed. Results: Cerebral ischemia/reperfusion resulted in the increase of intraneuronal free calcium content and activation of PKC. Dengzhanhua could prevent this change. Conclusion: PKC plays an important role in ischemic neuronal injury through inducing calcium overload.
出处
《第三军医大学学报》
CAS
CSCD
北大核心
2000年第1期12-14,共3页
Journal of Third Military Medical University
基金
国家自然科学基金!39670269
关键词
钙超载
蛋白激酶C
抑制剂脑缺血
大鼠
突触
calcium overload
protein kinase C
cerebral ischemia/reperfusion
