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.