中文摘要：

目的研究大鼠脑缺血再灌注后脑组织线粒体中信号转导和激活子3（STAT3）的表达情况，探讨线粒体中磷酸化STAT3（p-STAT3）与脑缺血后线粒体损伤的关系。方法：线栓法制作大鼠脑局部缺血再灌注模型，大鼠随机分为假手术（SHAM）组和大脑中动脉栓塞再灌注（I／R）组。透射电镜观察皮质区神经元内的线粒体损伤情况。Western blotting及免疫荧光双标法检测线粒体中STAT3及p-STAT3表达。结果：与SHAM组比较，大鼠脑缺血再灌注后，皮质区神经元内的线粒体损伤严重；线粒体中存在STAT3表达，且在脑缺血再灌注后表达量无变化，差异没有统计学意义（P〉0．05），而p-STAT3表达显著增加，差异具有统计学意义（P〈0．05）。结论：STAT3在大鼠脑组织线粒体中表达，脑缺血再灌注后被显著激活，推测脑缺血再灌损伤后，线粒体中STAT3的激活可能参与了脑缺血再灌注病理生理过程中线粒体的损伤和修复。

英文摘要：

Objective To assess the expression and activation of signal transducer and activator of transcription 3 （STAT3） inmitochondria of rat brain cortex, and explore the role of phosphorylated STAT3 （p-STAT3） in mitoehondrial injury and repair followingcerebral isehemia -reperfusion. Methods： The model of focal cerebral ischemia-reperfusion was established by suture method. The ratswere randomly divided into the sham-operated （SHAM） group and the middle cerebral occlusion-reperfusion （I/R） group. The uhrastructureof cortex mitoehondria was observed under transmission electronic microscope. The expressions of total STAT3 and p-STAT3 were detectedby western blotting and immunofluorescent double-staining. Results： A significant mitochondrial ultrastructural injury was found in I/Rgroup, compared with the SHAM group. STAT3 immunoreaetivity was observed in the mitochondria of rat brain cortex. No significantdifference in total STAT3 level was detected in both experimental groups （P〉0.05）, whereas the level of p-STAT3 in the mitochondria ofbrain cortex was elevated after isehemia injury （P〈0.05）. Conclusion： STAT3 localizes in mitoehondria. The activity of mitochondrialSTAT3 is elevated during cerebral ischemia-reperfusion. STAT3 activation may be involved in mitochondrial injury and repair in thepathophysiologieal process of cerebral ischemia-reperfusion injury.