氟伐他汀对心肌梗死后心力衰竭大鼠心肌单核细胞趋化蛋白-1表达的影响

目的:探讨羟甲基戊二酰辅酶A还原酶抑制剂氟伐他汀对急性心肌梗死(AMI)后心力衰竭(心衰)大鼠心肌单核细胞趋化蛋白-1(MCP-1)表达变化的影响。方法:雌性SD大鼠AMI术后6h随机分为:AMI对照组;氟伐他汀组;假手术组。直接灌胃给药8周后行高频多普勒超声、血流动力学、心脏重塑指标和左心室非梗死区心肌MCP-1mRNA表达的测定。结果:与假手术组比较,AMI组左心室舒张末期内径(LVEDD)、左心室舒张末期容积(LVEDV)、E峰、E峰减速度、E/A、左心室舒张末压(LVEDP)、左心室、右心室心肌肥厚指数、左心室非梗死区胶原容积分数(CVF)和MCP-1mRNA表达均显著增加(P<0.01),左心室短轴速短率(FS)和射血分数(EF)均显著降低(P<0.01)。与AMI组比较,氟伐他汀组的LVEDD、LVEDV、E峰、E峰减速度、E/A、LVEDP和左心室、右心室心肌肥厚指数、CVF和MCP-1mRNA表达均显著降低(P<0.01),FS和EF显著升高(P<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肌梗死后心衰大鼠心肌MCP-1的表达,抑制炎症反应。

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

Objective:To investigate the effect of fluvastatin on the expression of monocyte chemotactic protein-1(MCP-1)mRNA of myocardial tissue in rats with heart failure after acute myocardial infarction(AMI)Method:Six hours after ligating left coronary artery,surviving AMI female SD rats were randomly assigned to:1.AMI control;2.fluvastatin;3.sham-operated group are selected randomly as non-infarction control.After 8 weeks of therapy,We assessed cardiac function,hemodynamics,ventricular remodeling parameters,MCP-1 mRNA in left ventricular(LV)non-infarcted area(NIA).Result:Compared with 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 MCP-1 mRNA in NIA were all significantly increased in AMI group(P<0.01),while fractional shortening(FS)and ejection fraction(EF)were all significantly decreased(P<0.01).In comparison with AMI group,LVEDD,LVEDV,E-wave,E-wave deceleration,E/A,LVEDP,LVRW,RVRW,CVF and MCP-1 mRNA were all significantly decreased(P<0.01),while FS and EF were all significantly increased in fluvastatin group(P<0.01).Conclusion:Fluvastatin can attenuate LV remodeling and heart failure after AMI in the rat,Partly through down-regulating the expression of MCP-1 mRNA and improving inflammatory response.