Abstract
The aim of this study was to investigate the action of miR-93-5p in sevoflurane (Sev) preconditioning to protect against hypoxia/reoxygenation (H/R)-induced myocardial cell injury. H9c2 cells were preconditioned with Sev at concentrations of 1%, 2% and 4%, and subjected to H/R induction to establish the model. RT-qPCR was used to test miR-93-5p and NPAS2 levels. CCK8 assay and flow cytometry were used to detect cell viability and apoptosis. ELISA assays were used to measure myocardial injury markers (cTnI, CK-MB, MYO), as well as inflammatory factors (IL-6, IL-β, TNF-α). SOD and MDA kits were performed to detect oxidative stress levels. To investigate the impact of miR-93-5p on the protective effects of Sev pretreatment, we conducted transfection of miR-93-5p mimic. The connection of miR-93-5p with NPAS2 was confirmed using luciferase reporter gene assay. Our findings revealed that H/R treatment reduced cell viability, but Sev pretreatment enhanced it. In addition, Sev preconditioning reduced H/R-induced apoptosis, cTnI, CK-MB, MYO, MDA, IL-6, IL-β, and TNF-α levels, while elevated SOD levels. The miR-93-5p levels elevated with prolonged hypoxia time, but decreased with higher Sev pretreatment concentration. Transfection of miR-93-5p mimic attenuated protective efficacy by Sev preconditioning in myocardial cells. Besides, miR-93-5p targeted NPAS2 and negatively regulated it. In conclusion, our study demonstrated that sevoflurane preconditioning attenuated H/R-induced myocardial cells injury by modulating miR-93-5p.