芪苈强心调节急性心肌梗死大鼠心肌TNF-α和IL-10表达

Qiliqiangxin regulates TNF-α and IL-10 expression in cardiac myocytes of the rats with acute myocardial infarction

目的:探讨中药芪苈强心对急性心肌梗死(Acute myocardial infarction,AMI)大鼠心功能和炎症细胞因子TNF-α、IL-10表达的效用。方法:结扎大鼠左前降支,建立AMI模型。存活者随机分为梗死组(MI组)和芪苈强心治疗组(MI-Q组),另设假手术组(S组)。MI-Q组术后次日给予芪苈强心生药按4g/(kg·d)溶于生理盐水1.5ml治疗,MI组和S组仅以等量生理盐水同时间点灌胃,分别于术后第1、4周采用超声心动图和血流动力学检测心功能,实时定量PCR和免疫组织化学染色检测心肌组织中TNF-α和IL-10表达。结果:MI组大鼠左室功能明显减低,心肌细胞分泌的炎症因子TNF-α/IL-10比值明显升高。给予芪苈强心治疗后,心肌梗死大鼠心功能明显改善,心肌细胞表达TNF-α显著减少,IL-10表达显著增加。结论:减少心肌细胞促炎因子和增加抗炎因子的免疫调节作用可能是中药芪苈强心改善AMI大鼠心功能的免疫药理机制之一。

Objective ：The study is designed to explore the effects of traditional drug Qiliqiangxin on heart function and expression of proinflammatory cytokine tumor necrosis factor-or and anti-inflammatory cytokine interleukin-10 in rats with acute myocardial in- farction （AMI）. Methods：Rats with AMI were induced by left anterior descending branch ligation, and then were randomly divided into drug-treated group （MI-Q） and infarcted group （MI） compared with sham-operated group（S）. Rats in MI-Q group were treated with crude drug of Qiliqiangxin of4g/（kg ·d）dissolved in 1.5ml normal saline at next day after operation, while in the MI group and S group,the rats were treated with normal saline at the same time. Heart function of rats were detected at the end of 1st week and 4th week with eehocardiogram and hemedynamics. Myocardial cytokines including the pro-inflammatory cytokine tumor necrosis factor （TNF）-α and the anti-inflammatory cytokine： interleukin （IL）-10 were analyzed with real-time polymerase chain reaction （PCR）and immunohistochemical staining. Results： In AMI, the left ventricular function decreased, and the ratio of TNF-α/IL-10 in myocardium increased obviously. The cytokines were principally secreted by cardiac myocytes. The therapy of Qiliqiangxin markedly improved left heart function, reduced the production of TNF-α and increased IL-10 levels in cardiac myocytes. Conclusions：The immune regulatory effects of Qiliqiangxin concerns with attenuated production of pro-inflammatory cytokine and raised expression of anti-inflammatory cytokine,which should be one of the pharmacological mechanism of Qiliqiangxin to improve heart function of rats with AMI.