Sevoflurane alleviates hypoxia/reoxygenation-induced myocardial injury by regulating miR-208a-3p: an in vitro study

Abstract Objectives Myocardial hypoxia/reoxygenation (H/R) injury is a common pathological process in cardiovascular diseases. This study investigates whether sevoflurane alleviates H/R-induced myocardial injury by regulating miR-208a-3p and reveals the underlying molecular mechanisms. The findings may provide new therapeutic strategies for myocardial protection. Methods This study used neonatal rat cardiomyocytes as a model with 6-hour hypoxia treatment to simulate myocardial hypoxia. Cell viability was measured by CCK-8 assay, and miR-208a-3p expression levels were assessed by qRT-PCR. Inflammatory markers, myocardial injury markers, and oxidative stress markers were quantified by ELISA. The interaction between miR-208a-3p and its target gene was confirmed through dual-luciferase assays. Finally, the effects of sevoflurane and H/R treatment on the target gene were examined. Results This experiment found that the expression of miR-208a-3p reached its peak at 6 h of hypoxia. Sevoflurane preconditioning can concentration-dependently enhance cell viability, inhibit the upregulation of miR-208a-3p, and reduce the levels of myocardial injury markers cTnI and LDH. However, overexpression of miR-208a-3p inhibited cell activity, increased the levels of inflammatory, and promoted inflammatory responses. Meanwhile, overexpression of miR-208a-3p decreased SOD activity, increased MDA levels, and significantly enhanced oxidative stress. Mechanistically, sevoflurane enhances myocardial protection by targeting the 3′UTR of STC1 and upregulating STC1 expression. Conclusions Sevoflurane significantly alleviates H/R-induced myocardial injury by modulating miR-208a-3p, and this finding provides a new molecular target and potential therapeutic strategy for myocardial protection.