The aim of this study was to explore the effect of miR-26a-5p targeting and regulating ADAM17 gene on myocardial cells in hypoxic model. Myocardial cells from 1 day old Sprague-Dawley rats were isolated and cultured for 3 days, and were used for experiment. The hypoxia model of myocardial cells was established after cell grouping transfection. The targeting relationship between miR-26a-5p and ADAM17 was verified by bioinformatics website prediction and double luciferase report experiment. The double luciferase report experiment showed that miR-26a-5p had a targeted relationship with ADAM17, and miR-26a-5p could target and bind ADAM17, down-regulate its expression, and the transfection efficiency of each group was good (P < 0.05). After overexpression of miR-26a-5p, cell activity was increased (P < 0.05), apoptosis was decreased (P < 0.05), and the expression levels of TNF-α, IL-1β and IL-6 were significantly decreased (all P < 0.05). The release of creatine kinase-MB and the expression level of malondialdehyde were significantly decreased (both P < 0.05), and the expression level of superoxide dismutase was significantly increased (all P < 0.05). After overexpression of ADAM17, the results were reversed (all P < 0.05). MiR-26a-5p could target and regulate ADAM17, reduce the apoptosis of myocardial cells and the expression of inflammatory factors in acute myocardial infarction, and reduce the occurrence of oxidative stress.

这项研究的目的是探讨低氧模型中miR-26a-5p靶向和调节ADAM17基因对心肌细胞的作用。分离1天大的Sprague-Dawley大鼠的心肌细胞并培养3天，并用于实验。细胞分组转染后建立心肌细胞的低氧模型。通过生物信息学网站预测和双重荧光素酶报告实验验证了miR-26a-5p和ADAM17之间的靶向关系。双重荧光素酶报告实验表明，miR-26a-5p与ADAM17有针对性的关系，miR-26a-5p可以靶向并结合ADAM17，下调其表达，各组的转染效率均良好（P  <0.05 ）。miR-26a-5p过表达后，细胞活性增加（P <0.05），凋亡减少（P  <0.05），TNF-α，IL-1β和IL-6的表达水平显着降低（所有P  <0.05）。肌酸激酶-MB的释放和丙二醛的表达水平显着降低（均P  <0.05），超氧化物歧化酶的表达水平显着升高（均P  <0.05）。ADAM17过表达后，结果相反（所有P  <0.05）。MiR-26a-5p可以靶向和调节ADAM17，减少急性心肌梗死中心肌细胞的凋亡和炎性因子的表达，并减少氧化应激的发生。