Sevoflurane reduces cardiomyocyte injury in a hypoxia/reoxygenation model of cardiomyocytes through the linc01278/miR-134-5pt regulatory axis.

BACKGROUND: Ischemia-reperfusion leads to varying degrees of myocardial cell injury. Notably, long noncoding RNA was associated with the protective effect of sevoflurane (Sev) preconditioning against myocardial ischemic injury. Therefore, we further investigated the protective mechanism of Sev-mediated linc01278 against damaged cardiomyocytes by constructing a hypoxia/reoxygenation (HR) model of cardiomyocytes. METHODS: The expression of linc01278, miR-134-5p, and apoptotic biomarkers in cardiomyocytes was detected by RT-qPCR. The proliferation was detected by CCK8; apoptosis was observed by flow cytometry; and the degree of cardiomyocyte injury and the level of oxidative stress was observed by ELISA. Dual luciferase reporter assay and RIP verified linc01278 and miR-134-5p interactions. RESULTS: linc01278 was down-regulated in the HR group and up-regulated after Sev pretreatment. Sev markedly mitigated the HR-impaired cell proliferation, reduced apoptosis, and oxidative stress, and downregulated the expression of myocardial injury markers including cTnI, CK-MB, and LDH. However, this protection was noticeably reversed by the downregulation of the linc01278 expression. Mechanistically, linc01278 binds to miR-134-5p. miR-134-5p was highly expressed in cardiomyocytes of the HR, and lowly expressed in the Sev groups. The cardioprotective effect of Sev weakened by si-linc01278 was typically restored by miR-134-5p inhibitor. CONCLUSIONS: Sev attenuates HR-stimulated myocardial injury through linc01278/miR-134-5p axis-mediated proliferation, apoptosis, and oxidative stress.