Effect of miR-26a-5p targeting ADAM17 gene on apoptosis, inflammatory factors and oxidative stress response of myocardial cells in hypoxic model.

Abstract

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.