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

ABSTRACT 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.