白杨素改造物对急性心肌梗死小鼠心脏的影响

Effect of chrysin modification on the heart of mice with acute myocardial infarction

目的 探讨白杨素改造物(chrysin modification,CM)对小鼠急性心肌梗死(Acute myocardial infarction,AMI)后心脏功能、心脏重构的影响及其机制。方法 将24只C57小鼠分为4组:Sham+PBS组、Sham+CM组、AMI+PBS组和AMI+CM组,建立AMI小鼠模型。术后第1天腹腔注射CM,连续2周,超声检测左室心脏功能;实时荧光定量PCR法检测炎症因子一氧化氮合成酶(inducible nitric oxide synthase,iNOS)、肿瘤坏死因子α(tumor necrosis factor α,TNF α)、重组人精酸酶1(arginine 1,Arg1)、缺氧诱导有丝分裂因子(found in inflammatory zone 1,Fizz1)的mRNA水平;蛋白质印迹法检测iNOS和Arg1蛋白水平。结果 Sham+PBS组、Sham+CM组心脏功能指标无异常、心肌细胞排列整齐、无纤维化,炎症因子表达正常。与AMI+PBS组比,AMI+CM组的上述各指标均显著改善,心脏功能指标射血分数(ejection fraction,EF)和缩短分数(fractional shortening,FS)显著改善(P<0.05),小鼠心肌细胞排列趋于规则,细胞间隙明显缩小,iNOS、TNF α、Arg1和Fizz1的mRNA水平以及iNOS和Arg1的蛋白质水平差异均无统计学意义(均P>0.05)。结论 CM具有提高AMI后小鼠心脏功能、改善其心脏重构的作用,但不是通过调节巨噬细胞表型转换来实现的。

Objective To investigate the effect of chrysin modification(CM)on cardiac function and cardiac remodeling after acute myocardial infarction(AMI)in mice and its mechanism.Methods According to body weight,24 C57 mice were randomly divided into 4 groups:a sham+PBS group,a sham+CM group,an AMI+PBS group,and an AMI+CM group.CM was injected intraperitoneally 1 day after operation,and was continuously administered for 2 weeks.Left ventricular cardiac function was measured.The mRNA levels of nitric oxide synthase(iNOS),tumor necrosis factorα(TNFα),arginine 1(Arg1)and found in inflammatory zone 1(Fizz1)in heart tissues were analyzed by real-time RT-PCR.The protein levels of iNOS and Fizz1 in heart tissues were analyzed by Western blotting.Result The weight of mice in the sham+PBS group and the sham+CM group was normal.The myocardial cells were orderly arranged,and the expression of inflammatory factors was normal.Compared with the AMI+PBS group,the above indexes of the AMI+CM group were significantly improved,the ejection fraction(EF)and fractional shortening(FS)values were significantly increased(P<0.05),the arrangement of myocardial cells in mice tended to be regular,and the cell gap was significantly reduced.There was no significant difference among the mRNA level of iNOS,TNFα,Arg1 and Fizz1,and the protein expression of iNOS and Arg1(all P>0.05).Conclusion CM can improve cardiac function,but its protective effect is not achieved by regulating the phenotype conversion of macrophages.