中文摘要：

目的探讨抑制磷酸腺苷活化蛋白激酶（AMPK）活性对小鼠脑缺血再灌注损伤后神经元的保护作用机制。方法54只雄性C57BL／6小鼠，按随机数字表法分为假手术组、缺血再灌注组、缺血再灌注治疗组，每组18只。后2组采用线栓法建立小鼠大脑中动脉闭塞（MCAO）模型，缺血再灌注治疗组在插入线栓时腹腔注射AMPK抑制剂CompoundC，假手术组及缺血再灌注组相同时间予腹腔注射等量生理盐水。应用HE染色观察3组小鼠缺血再灌注后组织病理学变化；应用免疫组化染色法、TUNEL染色法观察脑缺血再灌注损伤24h后细胞色素C（CytC）的表达及神经元凋亡情况。结果与缺血再灌注组比较，缺血再灌注治疗组小鼠皮质及海马CA1区组织病理学损伤减轻，CytC阳性细胞数分别为（28．86±9．65）个／视野、（13．33±2．75）个／视野，差异均有统计学意义（P〈0．05）；TUNEL阳性细胞数亦显著减少。结论抑制AMPK活性能够减轻脑缺血再灌注损伤，推测机制为通过抑制CytC表达减少神经元凋亡。

英文摘要：

Objective To investigate the effects of inhibition of adenosine monophosphate-activated protein kinase （AMPK） activity on neuronal apoptosis in mice after cerebral ischemia reperfusion injury. Methods Fifty-four male C57BL/6 mice were randomly divided into three groups （n=18）： sham-operated group, ischemia reperfusion group and ischemia reperfusion therapy group. Mice models of middle cerebral artery occlusion （MCAO） in the later two groups were made by insertion of a thread through internal carotid artery. Compound C was injected intraperitoneally in ischemia reperfusion therapy group when the thread was inserted. The same volume of saline was given to the sham-operated group and ischemia reperfusion group at the same time to intraperitonel injection. The Cytochrome C （Cy C） expression and neuronal apoptosis were observed by immunohistochemical staining and TUNEL 24 h after cerebral ischemia reperfusion injury. Results As compared with that in the ischemia reperfusion group, the histopathological damage was reduced in the hippocampal CA1 region of mice in the ischemia reperfusion therapy group; Cyt C positive cells in the two groups were （28.86±9.65）/field and （13.33±2.75）/field, respectively. TUNEL positive cells in the two groups were （67.14±8.55）/HP and （74.57±6.77）/HP, with significant difference （P〈0.05）. Conclusion Inhibition of AMPK activity can decrease cerebral ischemia reperfusion injury, which is problely by lowering the Cyt C expression to decrease the neuronal apoptosis in mice.