羟基红花黄色素A改善SD大鼠心肌缺血/再灌注损伤

目的研究羟基红花黄色素A(hydroxysafflor yellow A,HSYA)对大鼠心肌缺血/再灌注(myocardial ischemia/reperfusion,MI/R)损伤的改善作用。方法采用结扎Sprague Dawley(SD)大鼠冠状动脉左前降支的方法,建立MI/R损伤模型;结扎大鼠冠状A前降支30 min,再灌注3 h,灌注即刻给药。实验分为假手术组(Sham组)、模型组(MI/R组)、HSYA治疗组(MI/R+HSYA组,5 mg/kg),每组10只动物。观察心肌缺血损伤面积大小、HE染色变化、心电图监测变化、心肌损伤标志物以及血清中IL-1、IL-6和TNF-α的含量变化。结果 MI/R+HSYA组心肌梗死面积显著低于MI/R组(P0.05)。HE染色显示MI/R+HSYA组心肌细胞形态更接近于假手术组。血流动力学及心电监测显示MI/R+HSYA组心肌舒缩功能指标左心室收缩末压(LVSP)、左心室上升最大速率(+dp/dtmax)、左心室下降最大速率(-dp/dtmax)以及心率(HR)较MI/R组均升高(P0.05)。MI/R+HSYA组血清肌酸激酶同工酶(CKMB)、肌钙蛋白I(c Tn I)水平较MI/R组有所降低(P0.05);IL-1、IL-6及TNF-α水平也较MI/R组有所降低(P0.05)。结论 HSYA可以降低心肌梗死的程度和范围,改善心功能,减少心肌细胞损伤,抑制炎症因子的释放,从而发挥保护和改善心肌缺血的作用。

Hydroxysafflor yellow A for ameliorating injury of myocardial ischemia/reperfusion in SD rats

Objective To study the effect of hydroxysafflor yellow A （HSYA） in ameliorating the injury of myocardial ischemia/reperfusion （MI/R） in rats.Methods The model of MI/R injury was established in SD rats through ligation of left anterior descending coronary arteries for 30 min and reperfusion for 3 h. All rats were divided into sham-operation group （Sham group）, model group （MI/R group） and HSYA group （5 mg/kg, each n=30）. The changes of myocardial infarction area, hematoxylin-eosin （HE） staining, electrocardiogram （ECG）, myocardial injury markers and inflammatory cytokines （IL-1, IL-6 and TNF-α） were observed.Results The myocardial infarction area was significantly smaller in HSYA group than that in MI/R group （P〈0.05）. HE staining showed that myocardial cell morphology in HSYA group was similar to that in Sham group. The monitoring of hemodynamics and ECG showed that LVSP, ＋dp/dtmax, -dp/dtmax and heart rate （HR） were all higher in HSYA group than those in MI/R group （P〈0.05）. The levels of creatine kinase MB （CK-MB） and cardiac troponin I （cTnI） decreased in HSYA group compared with MI/R group （P〈0.05）, and levels of IL-1, IL-6 and TNF-α decreased too in HSYA group compared with MI/R group （P〈0.05）.Conclusion HSYA can reduce the severity and range of myocardial infarction, improve heart function, inhibit inflammatory cytokine release, and play a role of protecting and ameliorating myocardial ischemia.