【摘要】 目的　探讨半胱天冬酶 - 3(Caspase- 3)抑制剂 (Ac- DEVD- CHO)对大鼠局灶性脑缺血的神经保护作用及其机制。方法　线栓法制备大鼠大脑中动脉闭塞 (MCAO)模型 ,利用 Bederson法评价神经体征 ,免疫组化检测 CPP32蛋白表达 ,利用 TUNEL染色和梗死面积来评价神经细胞损害。结果　脑室内给予 Ac- DEVD- CHO(1 60 ng)可明显减少 CPP32蛋白的表达 ,减少 TUNEL阳性细胞数 ,减少脑梗死面积 ,并可显著促进大鼠脑缺血后神经功能缺失的恢复。结论　 Ac- DEVD- CHO可能通过减少 CPP32蛋白的表达 ,减少神经细胞凋亡 ,对缺血性神经元起到保护作用。更多还原

【Abstract】 Objective To investigate the protective effect of Caspase-3 inhibitor (Ac-DEVD-CHO) against neuronal injury and the possible mechanisms, which mediate neuronal cell death following focal cerebral ischemia in rats. Methods The model of transient focal cerebral ischemia was made by occlusion of the middle cerebral artery (MCA) for 2 hours. Neurological deficits were evaluated by Bederson’s method, the expression of CPP32 protein was detected by immunohistochemistry method and the neuronal damage was assessed by TUNEL staining and infarct area.Results Ac-DEVD-CHO (160ng, intracerebroventricularly) could decrease the expression of CPP32 in the ischemia area remarkably, decrease neuronal apoptosis and infarct size and promote neurological function recovery significantly.Conclusions Ac-DEVD-CHO protected neurons against ischemia injury by reducing the expression of CPP32 and further decreasing neuronal apoptosis.更多还原