Abstract

To determine the relative expression of microRNA-499 after anoxia-reoxygenation injury and to investigate the anti-apoptotic regulatory mechanism. The anoxia-reoxygenation injury model of H9C2 cardiomyocytes was developed, including two groups; normoxia and anoxia-reoxygenation. Real-time polymerase chain reaction was used to detect the expression trend of microRNA-499 after hypoxia and anoxia-reoxygenation injury; different concentrations of microRNA-499 mimic were transfected and the cell survival was detected. The target gene of microRNA-499 was confirmed by luciferase reporter gene assay. The expression and effect on apoptosis were detected by real-time polymerase chain reaction and Western blot. The expression of microRNA-499 peaked at 24 h of hypoxia and 9 h of reoxygenation in H9C2 cardiomyocytes. MicroRNA-499 had an optimal protective effect against anoxia-reoxygenation injury when transfected at a concentration of 100 nm. In addition, microRNA-499 down-regulated the expression of target genes Jun N-terminal protein kinase and caspase-3 after anoxia-reoxygenation injury. Overexpression of microRNA-499 reduced anoxiareoxygenation- induced H9C2 cardiomyocyte injury, which may be related to the inhibition of apoptosis in H9C2 cardiomyocytes through the modulation of the Jun N-terminal protein kinase/caspase-3 pathway.