The SNHG10-miR-495-3p-PTEN axis is involved in sevoflurane-mediated protective effects in cardiomyocytes against hypoxia/reoxygenation injury

Myocardial infarction (MI) has been considered a leading cause of death worldwide. Relieving ischemia-reperfusion myocardial damage is one of the major roles in treating MI. Sevoflurane postconditioning provides myocardial protection, and this study probes the mechanism of sevoflurane-mediated protective effects. A hypoxia/reoxygenation (H/R) model was constructed in cardiomyocytes, which were pretreated with 2.4% sevoflurane. Alterations in SNHG10, miR-495-3p, and PTEN levels were determined, and gain- or loss-of functional assays were conducted to confirm the role of the SNHG10/miR-495-3p axis, which is potentially regulated by sevoflurane. Cell viability, oxidative stress, and inflammatory reactions were all evaluated. The results indicated that sevoflurane post-conditioning attenuated H/R-induced cardiomyocyte damage and reduced the SHNH10 level. SNHG10 overexpression reversed sevoflurane-mediated protective effects on cardiomyocytes. Moreover, SNHG10 targeted miR-495-3p and restrained its expression, while miR-495-3p targeted PTEN, suppressed PTEN levels, and promoted HIF-1α expression. miR-495-3p overexpression decreased SNHG10-mediated myocardial injury and enhanced HIF-1α levels. However, no additional protection was found when sevoflurane was administered to H/R-exposed cardiomyocytes following treatment with the HIF-1α inhibitor LW6. Overall, sevoflurane protects cardiomyocytes from H/R by modulating the SNHG10-miR-495-3p-PTEN-HIF-1α axis. •Sevoflurane suppresses hypoxia/reoxygenation-triggered myocardial cell damage.•Overexpressed SNHG10 abates the protective effect of sevoflurane on hypoxia/reoxygenation cardiomyocytes.•SNHG10 targets miR-495-3p and up-regulates PTEN.•Overexpressed miR-495-3p or inhibited HIF-1α attenuates the damaging effect of SNHG10 on H/R cardiomyocytes.