舒芬太尼后处理对大鼠心肌缺血再灌注时Ac—H3表达的影响

Effect of sufentanil postconditioning on Ac-H3 expression during myocardial ischemia-reperfusion in rats

目的评价舒芬太尼后处理对大鼠心肌缺血再灌注时乙酰化组蛋白I-13（Ac—H3）表达的影响。方法清洁级健康雄性sD大鼠36只，体重250～300g，采用随机数字表法分为3组（n=12）：假手术组（S组）、心肌缺血再灌注组（I／R组）和舒芬太尼后处理组（SP组）。采用结扎冠状动脉左前降支30min，再灌注120min的方法建立大鼠心肌缺血再灌注损伤模型。S组在冠状动脉左前降支下穿线，不结扎；SP组于再灌注前5min时股静脉注射舒芬太尼1μg／kg；S组和I／R组注射等容量生理盐水。于再灌注120rain时处死大鼠，取心肌组织，测定心肌梗死体积，计算心肌梗死体积百分比；采用TUNEL染色法检测心肌细胞凋亡情况，计算细胞凋亡指数；取心尖部组织，采用Western blot法检测Ac—H3的表达。结果与S组比较，I／R组和SP组心肌梗死体积百分比和细胞凋亡指数增加，Ae—H3表达水平降低（P〈0．05）；与I／R组比较，SP组心肌梗死体积和细胞凋亡指数降低，Ac—H3表达水平升高（P〈0．05）。结论舒芬太尼后处理可通过上调Ac—H3表达，恢复组蛋白乙酰化水平，从而减轻大鼠心肌缺血再灌注损伤。

Objective To evaluate the effect of sufentanil postconditioning on acetylated histon H3 （Ac-H3） expression during myocardial ischemia-reperfusion （I/R） in rats. Methods Thirty-six adult male Sprague-Dawley rats, weighing 250-300 g, were randomly divided into 3 groups （n = 12 each） using a random number table： sham operation group （ S group） , I/R group, and sufentanil postconditioning group （ SP group）. Myocardial I/R was induced by 30 min occlusion of the left anterior descending branch of the coronary artery followed by 120 rain reperfusion in anesthetized rats. Sufentanil 1 μg/kg was injected through the femoral vein at 5 rain before reperfusion in group SP, while the equal volume of normal saline was given in S and I/R groups. The rats were sacrificed at 120 min of reperfusion, and the myocardial specimens were obtained from the anterior wall of the left ventricle for determination of myocardial infarct size and cell apoptosis （by TUNEL） , and myocardial specimens were obtained from the apex for detection of Ac-H3 expression （using Western blot）. Apoptotic index was calculated. Results Compared with S group, the myocardial infarct size and apoptotic index were significantly increased, and Ac-H3 expression was down-regulated in I/R and SP groups （P〈0.05）. Compared with I/R group, the myocardial infarct size and apoptotic index were significantly decreased, and Ac-H3 expression was up-regulated in SP group （P〈 0.05）. Conclusion Sufentanil postconditioning attenuates myocardial I/R injury through up-regulating Ac- H3 expression and restoring histone acetylation in rats.