| Background:Ischemic heart disease is one of the diseases that endanger human health. After PCI and CABG treatment, restoration of epicardial coronary recanalization does not mean the realization of complete myocardial reperfusion and normal internal environment. There are still severe myocardial damage--ventricular remodeling (LVRM), after myocardial ischemia-reperfusion. The mechanism may be that the death of myocardial cells after reperfusion injury lead to myocardial remodeling. Therefore, the search to improve ventricular remodeling after reperfusion have a great significance for the treatment of ischemic heart disease. Certain genes that are expressed disorder lead to regulatory protein expression changes in cells, that may be the basis of pathological of cardiac remodeling occurs after reperfusion. So in gene level for clinical treatment of ventricular remodeling ventricular remodeling may provide new ideas. MicroRNAs (miRNAs) are found in eukaryotes, A variety of miRNAs have been confirmed to reduce ischemia-reperfusion myocardial injury. The miRNA-133a in myocardial mechanism of the proliferation and differentiation and cell apoptosis plays an important regulatory role. The study found that miRNA-133a can reduce ventricular remodeling after pressure overload and improve heart function. The purpose of this experiment is to research the role of miRNA-133a in the myocardial ischemia-reperfusion injury and to observe the expression of miRNA-133a in the ventricular remodeling after myocardial ischemia-reperfusion injury and to explore whether miRNA-133a participate in this process to preserved cardiac function.Methods:The model of myocardial ischemia-reperfusion injury in rats was constructed. Healthy adult male wistar rats were divided into five groups.(1) Sham group (2) I/R group (3) antagomiR-133a+I/R group (4) NS+I/R group and (5) Scramble+I/R group. In postoperative Id,3d,7d,15d, and30d, cardiac function was analyzed by echocardiography and biological and functional test systems. The myocardial samples were extracted. miRNA-133a levels were detected by quantitative reverse transcriptase-polymerase chain reaction (qRT-PCR). Histomorphology changes was observation by HE staining and myocardial fibrosis was evaluated by morphometric analysis. Western-bloting method was used to detect type I collagen protein expression and TUNEL staining was used to detect myocardial apoptosis.Results:In I/R group, with reperfusion time extension, cardiac function was gradually declined. The expression of type I collagen were significantly higher (p<0.05). Apoptosis were significantly increased (p<0.05). Ischemia area myocardial fibrosis was gradually worsened. miRNA-133a expression levels were markedly lowered(p<0.05). On the3d after reperfusion, apoptosis rate was highest (54.6%±7.3%), Fibrosis became obvious (I/R VS Sham:5.60%±2.30%VS1.64%±0.41%, p<0.05), and miRNA-133a was the lowest (0.540±0.134). agomiR-133a significantly increased myocardial miRNA-133a levels (p<0.01), inhibited myocardial apoptosis (p<.05), prevented myocardial fibrosis, lowered the expression of type I collagen and improved cardiac function.Conclusion:Fibrosis remodeling occurred after myocardial ischemia-reperfusion. The miRNA-133a expression was significantly lowered in the process of ventricular remodeling after myocardial ischemia-reperfusion injury. miRNA133a may be involved in the regulation of myocardial ischemia and reperfusion ventricular remodeling process. |
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