Uçar-Ekin, C.Oflazoğllu-Diken, H.Baksi, N.Aşır, F.Şahika-Gökdemir, G.2025-12-152025-12-1520250016-3813https://doi.org/10.24875/GMM.M25001025https://hdl.handle.net/20.500.12514/10065Background: Diabetes mellitus (DM) is a growing metabolic disease worldwide, associated with severe complications. Glucagon-like peptide-1 analogs and sodium-glucose cotransporter-2 inhibitors are promising therapeutic options for diabetic cardiomyopathy (DCM), although their cardioprotective mechanisms are not yet fully understood. Objective: This study evaluates the effects of liraglutide and empagliflozin on oxidative stress, inflammation, and histological changes in cardiac tissue in DCM. Materials and methods: Thirty-seven male Wistar albino rats were divided into four groups. Diabetes was induced in three groups using streptozotocin and nicotinamide. The groups were: (1) Control, (2) DM, (3) DM + Liraglutide (0.6 mg/kg, subcutaneously, 8 weeks), and (4) DM + Empagliflozin (30 mg/kg, oral gavage, 8 weeks). Blood samples were analyzed through enzyme-linked immunosorbent assay for tumor necrosis factor-α (TNF-α), interleukin-1 (IL-1), malondialdehyde (MDA), superoxide dismutase (SOD), advanced glycation end (AGE) products, and insulin. Cardiac tissue was examined histopathologically. Results: Diabetes significantly increased blood glucose, IL-1, TNF-a, MDA, and AGE (p < 0.01), while SOD levels decreased (p < 0.01), alongside myocardial damage. Liraglutide and empagliflozin improved all parameters (p < 0.01). Conclusion: Liraglutide and empagliflozin mitigate diabetes-induced cardiac damage, likely by reducing fibrosis, oxidative stress, and inflammation. © 2025 Academia Nacional de Medicina de México, A.C. Publicado por Permanyer.es10.24875/GMM.M25001025info:eu-repo/semantics/openAccessCardiovascular RiskDiabetic CardiomyopathyEmpagliflozinInflammationLiraglutideOxidative StressArticle2-s2.0-105022309718