中文摘要：

目的探讨Caspase-3激活和细胞色素c释放在脑缺血再灌注损伤后神经元细胞凋亡中的作用。方法利用MACo法建立小鼠急性脑缺血模型，以酶活性测定、Western杂交和免疫组化等方法对Caspase-3活性变化和激活以及细胞色素c释放进行规律性观察。结果①脑缺血再灌注损伤后3hCaspase-3活性即开始升高，并随时间延长而进一步升高，12—24h达到高峰；②脑缺血再灌注损伤后6hCaspase-3明显激活，手术组是假手术组的7．6倍（P〈0．01）；③脑缺血再灌注损伤后6h细胞色素c明显释放，手术组是假手术组的8．5倍（P〈0．01）。结论 脑缺血再灌注损伤后早期Caspase-3明显激活，细胞色素c明显释放，表明Caspase-3激活和细胞色素c释放参与了脑缺血再灌注损伤早期过程，有助于进一步研究脑缺血再灌注损伤的机制。

英文摘要：

Objective To evaluate the effects of caspase-3 activation and cytochrome c release in cerebral ischemia reperfusion induced neuronal cell death. Methods A focal cerebral ischemia C57L mice model was established by the middle cerebral occlusion （MACo） method. Caspase-3 activity was determined by an enzyme activity assay at different time points after ischemia reperfusion. Caspase-3 activation and cytochrome c release were determined by immunohistological staining and Western blot. Results （1）Caspase-3 activation immediately occurred at 3 h after ischemia repeffusion and was gradually increased to a peak at 12 h to 24 h. （2）Caspase-3 was significantly activated at 6 h after completion of ischemia repeffusion and it was increased by 7.6 times in comparison with the sham control （P 〈 0.01 ）. （3）Cytochrome c release occurred at 6h after completion of ischemia repeffusion and it was increased by 8.5 times in comparison with the sham control （ P 〈 0.01 ）. Conclusions Caspase-3 activation and cytochrome c release play a critical role in neuronal cell death induced by cerebral ischemeia reperfusion. This stuely provides insights into the mechanism of events involved in ischmeia reperfusion injury.