Propofol alleviates myocardial cell damage induced by myocardial ischemia–reperfusion injury via the miR-99a-5p/IGF1R pathway

This study aims to investigate the relationship between miR-99a-5p and Propofol (PRO) in myocardial ischemia–reperfusion injury (MIRI). Reverse transcription-quantitative polymerase chain reaction (RT-qPCR) was used to detect the expression of microRNA (miR)-99a-5p, insulin growth factor receptor (IGF1R), B-cell lymphoma 2 (Bcl2) and Bcl-2-associatred X protein (Bax) in a hypoxia/reoxygenation (H/R) model. The Cell Counting Kit-8 (CCK-8) assay and flow cytometry assay were employed to evaluate cell viability and apoptosis. Commercial kits were used to detect markers of myocardial injury and indicators of oxidative stress. The interaction between miR-99a-5p and IGF1R was validated by Dual luciferase reporter (DLR) and RNA immunoprecipitation (RIP) experiments. PRO treatment significantly inhibited H/R-induced myocardial cell apoptosis and oxidative stress. In the H/R model, PRO significantly downregulated the expression of miR-99a-5p and upregulated the expression of IGF1R. Overexpression of miR-99a-5p significantly counteracted the cardioprotective effects of PRO. Overexpression of IGF1R reversed the inhibitory effect of miR-99a-5p on PRO's protective effects, thereby alleviating myocardial cell damage. In conclusion, PRO may exert its cardioprotective effects by downregulating miR-99a-5p, which in turn upregulates IGF1R expression, thereby inhibiting apoptosis and alleviating oxidative stress, offering a new approach for the intervention of myocardial cell injury.