ArticleInternational journal of general medicine2026
Evaluating Semaglutide's Protection in H/R - Injured AC16 Cardiomyocytes: Oxidative Stress, Inflammation, Apoptosis, and Autophagy Insights.
Article in International journal of general medicine, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Objective: Semaglutide shows potential in cardiovascular protection, yet its specific role and mechanism in H/R injury are unclear. Given the role of autophagy in cardiomyocyte protection and the unclear mechanism of semaglutide in H/R - induced injury, this study aims to assess semaglutide's protective effects on AC16 cardiomyocytes in an H/R model and probe its mechanism, focusing on autophagy. Methods: AC16 cardiomyocytes were subjected to H/R to simulate H/R injury. Cells were divided into five groups: Control, H/R, H/R+Semaglutide, H/R+ Semaglutide+Rapamycin (autophagy activator), and H/R+Semaglutide+3-Methyladenine (3-MA, autophagy inhibitor). Cell viability, injury (LDH release), oxidative stress (MDA, SOD), and inflammation (IL-6, TGF-β) were assessed. Protein levels of cleaved caspase-3, caspase-9, Bax, Bcl-2, and the autophagy-related protein FUNDC1 were analyzed by Western blot. Results: H/R treatment significantly decreased cell viability and increased LDH release, indicating severe cellular injury ( Conclusion: Semaglutide shows substantial protective efficacy in safeguarding AC16 from H/R-triggered injury. It operates by mitigating oxidative stress, dampening inflammatory processes, inhibiting apoptotic pathways. Importantly, this investigation revealed that the cardioprotective effect, to a considerable degree, mediated through its promotion of autophagy.
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