Sevoflurane pretreatment attenuates hypoxia/reoxygenation injury in cardiomyocytes by regulating the GAS6-AS1/miR-483-3p/IGF1 axis

To investigate the role and mechanism of the lncRNA GAS6-AS1 in sevoflurane (Sev)-mediated cardio-protection against hypoxia/reoxygenation (H/R) injury in cardiomyocytes. AC16 cardiomyocytes were subjected to H/R injury (6 h hypoxia/24 h reoxygenation) and pretreated with Sev. RT‑qPCR was used to detect the level of GAS6-AS1, miR-483-3p, and IGF1. CCK‑8 and flow cytometry were applied to measure cell proliferation and apoptosis. ELISA determined myocardial injury markers, inflammatory factors, and oxidative stress levels. The targeting relationships were verified by dual‑luciferase reporter and RIP assays. GAS6-AS1 and IGF1 were downregulated, while miR-483-3p was upregulated in H/R‑treated cardiomyocytes. Sev pretreatment upregulated GAS6-AS1 and IGF1, downregulated miR-483-3p, promoted proliferation, inhibited apoptosis, and reduced myocardial damage, inflammation, and oxidative stress. Silencing GAS6-AS1 reversed the cardioprotective effects of Sev. GAS6-AS1 directly targeted miR-483-3p, which in turn directly inhibited IGF1. Inhibiting miR-483-3p restored IGF1 expression and reversed the detrimental effects of GAS6-AS1 silencing. Sev pretreatment protects cardiomyocytes against H/R injury by upregulating the GAS6-AS1/miR-483-3p/IGF1 axis, which offers a novel molecular target for perioperative cardio-protection. Not applicable.