Propofol has been revealed to protect cardiomyocytes against myocardial ischemia injury, although the underlying mechanism remains incompletely understood. H9C2 cells were used to generate a hypoxia/reoxygenation (H/R) in vitro model for the present study. Reverse transcription-quantitative PCR and western blotting were performed to measure the expression levels of microRNA (miR)-449a and nuclear receptor subfamily 4 group A member 2 (NR4A2). The CCK-8, BrdU, EdU, and caspase-3 activity assays and western blot analysis were employed to detect cell viability, proliferation, and apoptosis. The target relationship between miR-449a and NR4A2 was verified through dual-luciferase reporter assays. The results confirmed that exposure of the cells to H/R resulted in severe cell injury. However, the presence of propofol improved cell activity by promoting cell viability and proliferation and inhibiting cell apoptosis. The beneficial effect of propofol on H/R-mediated injury could be abrogated by the inhibition of NR4A2 mediated by miR-449a. Thus, the present study demonstrated that propofol counteracted cardiomyocyte H/R injury by inhibiting miR-449a to upregulate NR4A2.
Keywords: cardiomyocyte; hypoxia-reoxygenation; microRNA-449a; nuclear receptor subfamily 4 group A member 2; propofol.
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