Sevoflurane inhibits the apoptosis of hypoxia/reoxygenation-induced cardiomyocytes via regulating miR-27a-3p-mediated autophagy

Abstract

Abstract Introduction Sevoflurane (Sevo) prevents hypoxia/reoxygenation (H/R)-induced cardiomyocytes apoptosis. MiR-27a-3p expression is up-regulated in Sevo-treated hippocampal neurons. Objective This study explored whether the effect of Sevo on cardiomyocytes was mediated by miR-27a-3p. Methods The cardiomyocytes were cultured under H/R condition or pre-treated with Sevo, and further transfected with miR-27a-3p inhibitor or treated with an autophagy inhibitor 3-methyladenine (3-MA). Then the cell morphology was observed under an optical microscope. The cell viability and apoptosis were measured by MTT and flow cytometry. Expressions of miR-27a-3p, apoptosis-related, and autophagy-related factors were determined by western blot or RT-qPCR. Key findings Sevo improved the abnormal morphology, promoted the cell viability and the expressions of Bcl-2 and miR-27a-3p, but reduced the apoptosis and Bax and C-caspase-3 levels of H/R-induced cardiomyocytes. MiR-27a-3p inhibitor had an effect opposite to Sevo on the cardiomyocytes and further counteracted the effect of Sevo on the H/R-induced cardiomyocytes. Downregulation miR-27a-3p increased the expression of Beclin 1 and the ratio of LC3B-II to LC3B-I in H/R-induced cardiomyocytes. Furthermore, 3-MA had an opposite effect to miR-27a-3p inhibitor and further counteracted the effect of the miR-27a-3p inhibitor on H/R-induced cardiomyocytes. Conclusion Sevo inhibited the apoptosis of H/R-induced cardiomyocytes via regulating miR-27a-3p-mediated autophagy.