JAK2-STAT3通路介导缺血后处理心肌保护作用的初步研究

Role of the JAK2-STAT3 Pathway Mediates the Cardioprotection of Ischemic Postconditioning

目的:观察缺血后处理对大鼠心肌缺血再灌注损伤后心肌梗死面积及心肌细胞凋亡的影响,初步探讨其心肌保护的作用机制。方法:36只健康雄性Wistar大鼠(230～280g)随机平均分为3组,缺血再灌注(I-R)组,缺血后处理(Pos)t组,缺血后处理+AG490(JAK2-STAT3通路阻断剂)组(Post+AG490组)。I-R组缺血30min,再灌注120min。Post组缺血30min,再灌注120min,并于再灌注前实施缺血后处理(灌注10s,缺血10s)3个循环。Post+AG490组再灌注前5min静脉注射AG490,其他处理与Post组相同。再灌注120min后取心肌标本。TTC染色法检测心肌梗死面积;TUNEL法测定心肌细胞凋亡指数。结果:缺血后处理组与对照组相比心梗面积及心肌细胞凋亡指数明显降低(P<0.05)。AG490抑制了缺血后处理的心肌保护作用。结论:缺血后处理具有显著的心肌保护作用,这一作用是由JAK2-STAT3通路介导的。

Objective：To investigate the effect of ischemic postconditioning on myocardial infarction and myocardial apoptosis in ischemia-reperfusion injury of rats,and the protective mechanisms thereof. Methods：Thirty-six healthy male Wistar rats （230-280 g） were randomly divided into three groups,ischemia-reperfusion group （Group I-R）,ischemia 30 min and reperfusion 120 min without additional intervention; myocardial ischemic postconditioning group（Group Post）,after 30 min ischemia,the rats were comprised 3 cycles of 10 seconds reperfusion followed by 10 seconds ischemia,and then the rats were reperfused 120 min; myocardial ischemic postconditioning＋AG490 （JAK2-STAT3 pathway inhibitor） group （Group Post＋ AG490）,rats were treated with AG490 5 minutes before reperfusion,followed by myocardial ischemic postconditioning and 120 min reperfusion. The myocardial infarct size was measured by TTC staining. Apoptotic index of cardiomyocyte was detected by TUNEL. Results：Myocardial infarct size and myocardium apoptotic index were significantly reduced in Group Post compared to those in Group I-R （P〈0.05）. AG490 inhibited cardioprotective effect of ischemic postconditioning. Conclusion：Ischemic postconditioning provides potent cardioprotective effect. JAK2-STAT3 pathway mediates the cardioprotective effects of ischemic postconditioning.