【摘要】 目的 探索局灶脑缺血/再灌注不同时间诱导大鼠缺血中心区(同侧皮层)和周围区(同侧纹状体)信号转导与转录激活子-1(STAT1)的激活变化。方法 采用SD雄性大鼠线栓法制作右大脑中动脉缺血(MCAO)局灶脑缺血模型。运用抗STAT1和抗磷酸化STAT1抗体做免疫印迹(IB)检测缺血2h再灌注不同时间缺血中心区和周围区STAT1的表达及激活变化。结果 缺血2h再灌注不同时间，缺血中心区及周围区STAT1的磷酸化水平显著增加，再灌注24h达到峰值，与假手术组相比分别增加约3.1和3.8倍(P<0.05)，但在整个再灌注过程中其蛋白表达并没有明显的变化。结论 局灶脑缺血再灌注能引起缺血中心区和周围区STAT1磷酸化水平的显著增加，提示缺血性脑损伤诱导STAT1的激活可能参与缺血同侧皮层及纹状体神经元细胞的病理生理过程。

    【关键词】 MCAO；局灶脑缺血；信号转导与转录激活子-1(STAT1)

    【Abstract】 Objective To investigate the activation of signal transducer and activator of transcription-1(STAT1) after focal brain ischemia in the lesion core (cerebral cortex) and lesion periphery(striatum). Methods Middle cerebral artery occlusion (MCAO) ischemia model of SD rats was used in this study. The content of STAT1 protein and changes of p-STAT1 in the cerebral cortex and striatum homogenates were assessed by immunoblotting(IB) using anti-STAT1 and anti-p-STAT1 (Tyr 701) antibodies.Results The expression of STAT1 protein was not significantly altered during ischemia 2h and reperfusion different time, but phosphorylation levels of STAT1 was continuously increased and peaked at 24h of reperfusion in the cortex and striatum (3.1-and 3.8-folds vs sham respectively). Conclusion The activation of STAT1 was induced in the lesion core and lesion periphery following focal cerebral ischemia. The increments of p-STAT1 could involve in the changes of pathophysiology in the nervous cells. ......