The Preconditioning with Sevoflurane Alleviates Hypoxia-Reoxygenation-Induced Myocardial Cell Injury by Regulating the lncRNA LINC00265/miR-370-3p Axis.

Abstract

In recent years, the cardioprotective effects of the volatile anesthetic sevoflurane (SEV) have been confirmed, yet its underlying molecular mechanisms remain incompletely elucidated. Notably, lncRNA LINC00265 has been identified as dysregulated in damaged cardiomyocytes, potentially contributing to disease progression. However, limited research has focused on the interplay between SEV and lncRNA LINC00265. The main objective of this study was to explore the mechanism and role of lncRNA LINC00265 in mediating the cardioprotective effects of SEV against myocardial injury. An in vitro hypoxia/reoxygenation (H/R) model was created in AC16 cells following pretreatment with varying concentrations of SEV. RT-qPCR was used to evaluate the levels of lncRNA LINC00265, miR-370-3p, IL-6, and TNF-α. The concentrations of CK-MB and cTnI were determined using ELISA. Cell viability was evaluated using CCK-8, and apoptosis was quantified by flow cytometry. Additionally, the relationship between lncRNA LINC00265 and miR-370-3p was confirmed using a dual-luciferase reporter assay. Prolonged hypoxia gradually rose in lncRNA LINC00265 levels, which was reversed by SEV pretreatment. SEV pretreatment mitigated H/R-induced decreases in cell viability, increases in apoptosis, and excessive production of IL-6, TNF-α, CK-MB, and cTnI. However, the protective effects of SEV were counteracted by lncRNA LINC00265 overexpression. A negative regulatory relationship between lncRNA LINC00265 and miR-370-3p was discovered. miR-370-3p overexpression mitigated diminished protective effects of SEV by elevated lncRNA LINC00265 in myocardial injury. lncRNA LINC00265 could diminish the protective effects of SEV against myocardial injury by functioning as a sponge for miR-370-3p.