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功能评分、脑梗死体积及神经元凋亡的影响。方法72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24只。后两组采用线栓法建立小鼠大脑中动脉闭塞（MCAO）模型，其中缺血再灌注治疗组在插入线栓时腹腔注射AMPK抑制剂CompoundC．缺血再灌注组于同等时间给予等量生理盐水腹腔注射。在小鼠脑缺血再灌注损伤后24h，采用Longa法测定各组大鼠神经功能缺损评分，采用2，3，5-三苯基氯化四氮唑（TTC）染色测量脑梗死体积，采用TUNEL染色法观察神经元凋亡情况。结果与缺血再灌注组相比[（2．10±0．24）分；43．10％±11．50％；皮质：（81．00±12．21）个／视野，海马：（56．00±5．29）个／视野]相比，缺血再灌注治疗组神经功能缺损评分[（1．58±0．22）分】、脑梗死体积（24．84％±12．53％）及神经元凋亡数量[皮质：（58．86±9．65）个／视野，海马：（43．33±3．79）个／视野]均明显减少，差异均有统计学意义（P〈0．05）。结论抑制AMPK活性能减少小鼠脑缺血再灌注损伤后的神经元凋亡，具有神经保护作用。

英文摘要：

Objective To observe the effect of inhibition of AMP-activated protein kinase （AMPK） activity on neurological deficits, infarct volumes and neuronal apoptosis after cerebral ischemia reperfusion injury in mice. Methods Seventy-two male C57BL/6 mice were randomly divided into three groups （n=24）： the sham-operated group, the ischemia reperfusion group and the ischemia reperfusion＋treatment group. Mice models of middle cerebral artery occlusion （MCAO） were established by insertion of a thread through internal carotid artery. AMPK inhibitor Compound C was injected intraperitoneally in the mice of ischemia reperfusion＋treatment group when the thread was inserted; the same volume of saline was given to ischemia reperfusion group at the same time. Twenty-four h after cerebral ischemia reperfusion, neurological deficits were observed by Longa method; infarct volumes were measured by TTC staining and neuron apoptosis was observed by TUNEL. Results there was a significant reduction in ischemia reperfusion＋treatment group in terms of neurological deficits （[1.58± 0.22] points vs. [2.10±0.24] points） and infarct volume of ischemia （24.84%± 12.53% vs. 43.10%± 11.50%） and cell number of neuron apoptosis （cortex： [58.86±9.65]/field vs. [81.00±12.21]/field; hippocampus： [43.33±3.79）]/field vs. [56.00±5.29J/field） as compared with ischemia reperfusion group （P〈0.05）. Conclusion Inhibition of AMPK activity may reduce neuron apoptosis, having neuro-protective role.