脑缺血-再灌注诱导大鼠皮层和纹状体组织信号转导与转录激活子-3的激活变化

STAT3 was induced following middle cerebral artery occlusion in the cerebral cortex and striatum of SD rats

目的研究局灶脑缺血诱导大鼠皮层和纹状体信号转导与转录激活子-3(STAT3)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STAT3和抗磷酸化STAT3抗体做免疫印迹(IB)检测皮层和纹状体STAT3的表达及激活变化。结果缺血-再灌注不同时间并不能引起皮层及纹状体STAT3蛋白表达变化,但可诱导其磷酸化水平显著增加。缺血-再灌注24h达到峰值,与假手术组相比分别增加约5.5倍和8.4倍。结论局灶脑缺血-再灌注能引起缺血同侧皮层和纹状体STAT3磷酸化水平的显著增加,提示缺血性脑损伤诱导STAT3的激活可能参与缺血皮层区和纹状体神经元细胞的病理生理过程。

Objective To investigate the activation of signal transducer and activator of transcription-3（STAT3） alter focal brain ischemia. Methods Middle cerebral artery occlusion （MCAO） ischemia model of SD rats was used in this study. The content of STAT3 protein and changes of p-STAT3 in the lesion core （cerebral cortex） and lesion periphery（striatum） homogenates extracts were assessed by immunoblotting（IB） using anti-STAT3 and special anti-p-STAT3 （Tyr 705） antibodies. Results Phosphorylation levels of STAT3 was continuously increased after 0.5h of reperfusion and peaked at ischemia/reperfusion （I/R） 24h in the cortex and striatum （5.5-and 8.4-folds vs control, respectively） but the variation of STAT3 protein expression was not significant during I/R. Conclusion The activation of STAT3 was induced in the lesion core （cortex） and lesion periphery （striatum） following fobal cerebral ischemia. The increments of p-STAT3 could be involved in the changes of pathophysiology in the cortex and striatum nervous cells.