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目的观察大鼠心肌梗死(MI)后MI交界区微小RNA-126(miR-126)及血管内皮生长因子(VEGF)表达的动态表达变化,初步探讨miR-126及VEGF对缺血局部血管新生的影响。方法雄性SD大鼠结扎冠状动脉左前降支建立急性心肌梗死模型组(AMI组),另设假手术对照组(Sham组),每组30只。于术后7 d、14 d和28 d分别处死10只大鼠,进行MI面积百分比测定,实时荧光定量PCR法检测心梗交界区miR-126、VEGF mRNA表达水平,免疫组织化学方法检测各组大鼠MI交界区VEGF蛋白的表达。结果 Sham组术后7 d、14 d和28 d心肌组织miR-126mRNA和VEGF mRNA的表达均无明显区别,AMI组术后7 d、14 d和28 d,MI交界区mir-126 mRNA表达与相应的Sham组相比,均有不同程度的下降(P<0.01),而VEGF mRNA的表达则均有不同程度的增高(P<0.01);在AMI组,随着MI时间的延长,miR-126和VEGF mRNA的表达均逐渐升高,且在AMI 14 d达到高峰(P<0.05)。VEGF的蛋白表达情况与其基因表达基本一致。结论大鼠MI后VEGF mRNA及其蛋白的表达明显升高的同时伴随miR-126基因表达的降低,随着缺血时间延长,miR-126 mRNA表达有所恢复。
Objective To investigate the dynamic expression of microRNA-126 (miR-126) and vascular endothelial growth factor (VEGF) in the MI junction after myocardial infarction (MI) in rats and to explore the possible role of miR-126 and VEGF in ischemic local angiogenesis influences. Methods Acute myocardial infarction model group (AMI group) was established by ligation of the left anterior descending branch of coronary artery in male Sprague Dawley rats. Sham group (30 rats in each group) was also established. 10 rats were sacrificed on the 7th, 14th and 28th day after operation, respectively. The area percentage of MI was measured. The expression of miR-126 and VEGF mRNA were detected by real-time fluorescence quantitative PCR. The expression of VEGF mRNA was detected by immunohistochemical method Expression of VEGF protein in rat MI junction. Results There were no significant differences in the expression of miR-126 mRNA and VEGF mRNA in myocardium between the Sham group and the MI group at 7 d, 14 d and 28 d after operation (P <0.01), while the expression of VEGF mRNA increased in different degree (P <0.01). In AMI group, with the increase of MI time, miR- 126 and VEGF mRNA expression gradually increased, and peaked on the 14th day of AMI (P <0.05). VEGF protein expression and its gene expression are basically the same. Conclusions The expression of VEGF mRNA and protein is significantly increased after MI in rats, accompanied with the decrease of miR-126 gene expression. With the prolongation of ischemia, the expression of miR-126 mRNA is restored.