氟伐他汀对心肌梗死后心衰大鼠白介素-1β表达的影响

目的探讨羟甲基戊二酰辅酶A(HMG-CoA)还原酶抑制剂氟伐他汀对急性心肌梗死后心衰大鼠白介素-1β(IL-1β)表达变化的影响。方法♀SD大鼠急性心肌梗死(AMI)术后6 h随机分为:①AMI对照组;②氟伐他汀组;另设:③假手术组。直接灌胃给药8 wk后行高频多普勒超声、血流动力学、心室重塑指标、左室心肌IL-1βmRNA表达的测定。结果与假手术组相比,AMI组左室舒张末期内径(LVEDD)、左室舒张末期容积(LVEDV)、E峰、E峰减速度、E/A、左室舒张末压(LVEDP)、左、右心室心肌肥厚指数、非梗死区胶原容积分数(CVF)和IL-1βmRNA均增加(P均<0.01),左室短轴速短率(FS)和射血分数(EF)均降低(P均<0.01)。与AMI组相比,氟伐他汀组的LVEDD、LVEDV、E峰、E峰减速度、E/A、LVEDP和左、右心室心肌肥厚指数、CVF和IL-1βmRNA均降低(P均<0.01),FS和EF升高(P均<0.01)。结论氟伐他汀能有效抑制心室重塑,延缓心衰进展,其机制可能部分通过下调心梗后心衰大鼠心肌IL-1β的表达,改善炎症反应。

Effect of fluvastatin on the expression of myocardial IL-1β in rats with heart failure after acute myocardial infarction

Aim To investigate the effect of fluvastatin(FV)on the expression of IL-1β mRNA of left ventricular(LV) myocardium in rats with heart failure after acute myocardial infarction(AMI).Methods 6 h after ligating left coronary artery,surviving AMI female SD rats were randomly assigned to: ①AMI control;②AMI+FV;③sham-operated group,which was randomly selected as non-infarction control.After 8 weeks of therapy,we assessed cardiac function,hemodynamics,ventricular remodeling parameters and IL-1β mRNA expression in the infarcted and non-infarcted area(IA,NIA).Results Compared with the sham-operated group,LV end-diastolic dimension(LVEDD),LV end-diastolic volume(LVEDV),E-wave,E-wave deceleration,E/A ratio,LV end diastolic pressure(LVEDP),relative weight(LVRW),right ventricular relative weight(RVRW),collagen volume fraction(CVF) and IL-1β mRNA in NIA were all significantly increased in the AMI group(all P<0.01),while fractional shortening(FS) and ejection fraction(EF) were all significantly decreased(all P<0.01).In comparison with the AMI group,LVEDD,LVEDV,E-wave,E-wave deceleration,E/A,LVEDP,LVRW,RVRW,CVF and IL-1β mRNA in NIA were all significantly decreased(all P<0.01),while FS and EF were all significantly increased in the FV group(all P<0.01).Conclusion FV can attenuate LV remodeling and heart failure after AMI in rats,partly through down-regulating the expression of IL-1β mRNA and improving inflammatory response.