中文摘要：

目的探讨抑制磷酸腺苷活化蛋白激酶（AMP—activatedproteinkinase，AMPK）活性对小鼠脑缺血再灌注后细胞色素C（cytochromeC，CytC）和凋亡诱导因子（apoptosisinducingfactor，AIF）表达的影响。方法36只雄性C57BL／6小鼠随机分为假手术组、缺血再灌注组和CompoundC组，每组12只，每组分别有6只用于CytC和AIF免疫组化检测。线栓法建立大脑中动脉闭塞（middlecerebralarteryocclusion，MCAO）模型。治疗组在插入线栓时腹腔注射CompoundC，假手术组和缺血再灌注组在相同时间点腹腔注射等体积生理盐水。应用免疫组化染色法观察脑缺血再灌注24h时CytC和AIF表达。结果假手术组大脑皮质可见数个CytC[IH性细胞，CAl区未见CytC[IH性细胞。CompoundC组大脑皮质[（28．86±9．65）个／高倍视野对（58．86±9．65）个／高倍视野；t=7．615，P=0．000]和海马CAl区[（13．33±2．75）个／高倍视野对（43．33±3．79）个／高倍视野；t=22．194，P=0．000]CytC阳性细胞数量较缺血再灌注组均显著性减少。假手术组大脑皮质区未见AIF阳性细胞，海马CAl区可见数个AIF阳性细胞。CompoundC组大脑皮质[（32．16±2．35）个／高倍视野对（46．70±3．45）个／高倍视野；t=12．066，P=0．000]和海马CAl区[（13．17±3．91）个／高倍视野对（17．35±3．67）个／高倍视野；t=2．700，P=0．013]AIF阳性细胞数量较缺血再灌注组大脑皮质显著性减少。结论抑制AMPK活性可下调脑缺血再灌注后CytC和AIF的表达。

英文摘要：

Objeelive To investigate the effect of inhibiting adenosine monophosphate-activated protein kinase （AMPK） on the expressions of cytochrome c （CytC） and apoptosis-inducing factor （AIF） after cerebral ischemia-reperfusion in mice.Methods Thirty-six male C57BL/6 mice were randomly divided into three groups： A sham operation group, an ischemia-reperfusion group, and a compound C group （n = 12 in each group）. Six mice in each group were used for CytC and AIF immunohistochemical detection. A model of middle cerebral artery occlusion （MCAO） was induced by the intraluminal suture method. Compound C was injected intraperitoneaUy in the treatment group when the thread was inserted. The same volume of saline was injected intraperitoneally at the same time point in the sham operation group and theischemia-reperfusion group. At 24 hours after ischemla-reperfusion, the expression of CytC and AIF was observed by immunohistochemical staining. Results A number of CytC positive cells in cortex were seen in the sham operation group. No CytC positive cells were seen in the CA1 region. The number of CytC positive cells in the cerebral cortex （28.86 ± 9. 65/high power field vs. 58.86 ± 9. 65/high power field; t = 7. 615, P =0. 000） and hippocampal CA1 region （13.33 ± 2. 75/high power field vs. 43.33 ± 3.79/high power field; t = 22. 194, P =0. 000） in the compound C group were reduced significantly compared to those in the ischemia- reperfusion group. No AIF-positive cells were seen in the hippocampal CA1 region in the sham operation group. A number of AIF-positive cells were seen in the hippocampal CA1 region. The number of AIF- positive cells of cerebral cortex （32. 16 ± 2. 35/high power field vs. 46. 70 ± 3. 45/high power field; t = 1Z 066, P =0. 000） and hippocampal CA1 region （13. 17 ±3. 91 /high power field vs. 17.35 ±3. 67/high power field; t -2. 700, P =0. 013） in the compound C group were significantly reduced compared to those in the cortex of the ischemia- reperfusion group. Conc