Sevoflurane Mediates LINC00339/miR‐671‐5p/PSMB2 Axis to Improve Cardiomyocytes Against Hypoxia/Reoxygenation Injury

Ischemia/reperfusion (I/R) causes a deterioration in heart function, leading to myocardial infarction. It is aimed at investigating the protective mechanism of sevoflurane (Sevo) on cardiomyocytes by constructing a cellular model of hypoxic/reoxygenation (H/R) in this study.[Human hybrid] epithelioid cells (AC16) were induced by H/R to establish a model of myocardial I/R injury and Sevo postconditioning. The expression of long intergenic non-protein coding RNA 339 (LINC00339), microRNA-671-5p (miR-671-5p) and proteasome 20S subunit beta 2 (PSMB2) was detected by quantitative reverse transcription-polymerase chain reaction (qRT-PCR). Viability and apoptosis of AC16 cells were detected by cell counting kit-8 (CCK-8) assay and flow cytometry, respectively. The levels of interleukin-6 (IL-6), IL-10, tumor necrosis factor-a (TNF-a), reactive oxygen species (ROS), malondialdehyde (MDA), glutathione peroxidase (GSH-Px) and superoxide dismutase (SOD), were detected. LINC00339 expression was upregulated in H/R cardiomyocytes relative to the Control group, whereas Sevo decreased LINC00339 expression in H/R cardiomyocytes. The viability of AC16 cells were increased, and apoptosis, oxidative stress, and inflammatory responses decreased in the Sevo postconditioning group relative to the H/R group, but the protective effect of Sevo on H/R cardiomyocytes was partially reversed by LINC00339 overexpression. LINC00339 negatively regulated miR-671-5p, and miR-671-5p upregulation could alleviate the damage of LINC00339 on H/R cardiomyocytes. PSMB2, a downstream target gene of miR-671-5p, could inhibit the protective effect of Sevo on H/R cardiomyocytes. Sevo postconditioning exerts a protective effect in H/R-induced cardiomyocyte injury, which may be achieved by interfering with LINC00339/miR-671-5p/PSMB2 expression.