STAT3介导缺血后处理心肌保护作用的研究

目的研究大鼠心肌经历缺血再灌注损伤后心功能指标的变化，探讨缺血后处理是否具有保护作用，并探寻STAT3在其中的作用机制。方法SD大鼠32只，随机分为4组：对照组、缺血再灌注组、缺血后处理组、缺血后处理组＋NSC-74859（STAT3抑制剂）组。建立大鼠离体心脏工作模型，观察心脏在各组条件下心率、LVSP、＋dp／dtmax、-dp／dtmax、冠脉流量的变化及心肌酶谱的改变。结果缺血后处理组与缺血再灌注组相比，复灌期心率，冠脉流出液中CK及LDH的含量明显降低，左室收缩压、左心室压力变化率、冠状动脉流出量明显升高。而抑制STAT3表达后，此保护效应明显减弱。结论缺血后处理有助于减轻缺血再灌注所致心肌损伤，这一作用由STAT3转录因子介导。

Role of STAT3 mediates cardioprotection of ischemic postconditioning

Objective To research ischemic postconditioning on heart function after myocardial ischemia-reperfusion （I/R）, and the protective mechanisms. Methods Thirty-two rats were divided into four groups ： I/R group （ n = 8 ） , isehemic postconditioning group （ n = 8 ）, myocardial isehemic postconditioning ＋ NSC-74859 （ STAT3 inhibitor） group （ n = 8 ）, and control group （ n = 8 ）. Establish a model of rat to observe changes of the heart rate, LVSP, ＋ dp/dtmax, - dp/dtmax, coronary flow and myocardial enzyme spectrum in each group un-der different conditions. Results Compared with ischemia-reperfusion group, heart rate of the reperfusion period, CK and LDH of coronary ef-fluent in the ischemic posteonditioning group were obviously lower,while left ventricular systolic pressure, change of intraventricular pressure, and coronary effluent volume increased obviously. And after inhibition of STAT3 expression, this protective effect decreased significantly. Con-clusion Isehemic posteonditioning can provide potent eardioproteetive effect in which STAT3 mediates the eardioprotective effects.