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目的:探讨活血通络方通过线粒体途径抗大鼠脑缺血再灌注后神经元凋亡机制。方法:将大鼠随机分成假手术组、模型组、活血通络组,大脑中动脉栓塞再通法建立脑缺血再灌注模型。大鼠脑缺血再灌注6、12、24和48h不同时间点进行神经功能评分,并用原位末端标记法检测凋亡神经元,用免疫组化法检测Cyto-C、caspase-9、caspase-3阳性细胞数。结果:活血通络方对再灌注各时间点神经功能评分有不同程度的改善,能减少神经元凋亡指数和Cyto-C、caspase-9、caspase-3的表达(P<0.01~0.05)。结论:Cyto-C、caspase-9和caspase-3在脑缺血再灌注损伤中发挥重要作用,活血通络方能减轻缺血再灌注所致神经元凋亡,保护神经功能,其机理与抑制细胞凋亡线粒体通路有关。
Objective: To investigate the mechanism of Huoxuetongluo-induced neuron apoptosis after cerebral ischemia-reperfusion in rats through the mitochondrial pathway. Methods: Rats were randomly divided into sham operation group, model group, and Huoxuetongluo group. Cerebral ischemia-reperfusion model was established by middle cerebral artery embolization. Neurological function scores were performed at different time points of cerebral ischemia-reperfusion injury at 6, 12, 24, and 48 hours. Apoptotic neurons were detected by in situ end labeling. Cyto-C, caspase-9, and caspase- were detected by immunohistochemistry. 3 positive cell number. RESULTS: Huoxuetongluo prescription improved the neurological function score at different time points in reperfusion, and decreased the neuronal apoptosis index and the expression of Cyto-C, caspase-9 and caspase-3 (P<0.01-0.05). Conclusion: Cyto-C, caspase-9 and caspase-3 play an important role in cerebral ischemia-reperfusion injury. Huoxuetongluo can reduce the apoptosis of neurons induced by ischemia-reperfusion, protect the nerve function, its mechanism and inhibition. Apoptosis is related to mitochondrial pathways.