Arch Biochem Biophys. 2026 Mar 31:110803. doi: 10.1016/j.abb.2026.110803. Online ahead of print.
ABSTRACT
BACKGROUND: Myocardial ischemia-reperfusion injury (MIRI) represents a critical pathological challenge in cardiovascular disease treatment. Sevoflurane (Sev) preconditioning has been demonstrated to effectively mitigate MIRI, yet its specific molecular mechanism remains incompletely elucidated.
AIM: This study aims to investigate whether Sev preconditioning exerts myocardial protection by regulating the LINC00612/miR-331-3p/SOCS1 axis.
METHODS: AC16 cells were used to establish an H/R model to simulate MIRI, with pretreatment by Sev. RT-qPCR was used to detect the expression of LINC00612, miR-331-3p, and SOCS1 in cells. Cell viability and apoptosis were assessed by CCK8 assay and flow cytometry. Cardiac injury markers cTnⅠ and CK-MB, pro-inflammatory cytokines IL-6 and TNF-α, and oxidative stress markers MDA and SOD were detected by ELISA and related kits. The protein levels of SOCS1, Bax/Bcl-2, and p-STAT1/p-STAT3 were detected by Western blot. Dual-luciferase reporter assays were employed to identify the binding of miR-331-3p to LINC00612 and SOCS1.
RESULTS: H/R treatment reduced LINC00612 expression, while Sev pretreatment upregulated its expression. Sev preconditioning enhanced cell viability, inhibited apoptosis, and mitigated myocardial injury and inflammatory cytokine release, whereas silencing LINC00612 counteracted these protective effects. However, inhibition of miR-331-3p reversed cell injury caused by silencing LINC00612. Additionally, SOCS1 was found to have a direct targeting relationship with miR-331-3p.
CONCLUSION: Sev preconditioning may mitigate MIRI by modulating apoptosis, oxidative stress, and inflammatory responses through regulation of the LINC00612/miR-331-3p/SOCS1 axis.
PMID:41933859 | DOI:10.1016/j.abb.2026.110803