Isoflurane Preconditioning May Attenuate Cardiomyocyte Injury Induced by Hypoxia/Reoxygenation Possibly by Regulating miR-363-3p

• DOI: 10.1007/s12640-022-00584-6
• Publication Date: 2022-10-12T05:07:40Z
• Authors: Yanhu Ge; Chengbin Wang; Boqun Cui; Yaguang Liu; Duomao Lin; Liang Zhang; Liyun Zhao; Jun Ma
• Keywords: MicroRNAs; 03 medical and health sciences; 0302 clinical medicine; Isoflurane; Humans; Myocytes, Cardiac; Apoptosis; Hypoxia; Cell Hypoxia

This study attempted to explore whether miR-363-3p play a role in the isoflurane (ISO)-mediated protective effect of cardiomyocyte injury induced by hypoxia/reoxygenation (H/R). A myocardial cell injury model was established, and the different preconditioning ISO concentrations were screened and determined. The miR-363-3p level was detected by RT-qPCR. The effects of miR-363-3p on proliferation and apoptosis of H9c2 cells were detected by CCK-8 assay and flow cytometry. Myocardial injury indexes were determined by enzyme-linked immunosorbent assay (ELISA). The interaction of miR-363-3p with the 3'-UTR of the KLF2 gene was confirmed by luciferase reporter gene assay. ISO pretreatment can reduce the up-regulation of miR-363-3p after H/R injury. ISO pretreatment reduces the inhibition of cell viability and the promotion of cell apoptosis induced by H/R stimuli, while the overexpression of miR-363-3p counteracts the protective effect of ISO pretreatment. Meanwhile, ISO pretreatment also reduced the level of markers of H/R-induced myocardial injury. Moreover, luciferase reporter analysis showed that KLF2 was the downstream target gene of miR-363-3p. ISO pretreatment may alleviate H/R-induced cardiomyocyte injury by regulating miR-363-3p.