Liraglutide and empagliflozin alleviate diabetic cardiomyopathy by reducing oxidative stress and inflammation.

Background: 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 (AGEs) products, and insulin. Cardiac tissue was examined histopathologically.

Results: Diabetes significantly increased blood glucose, IL-1, TNF-α, MDA, and AGEs (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.