Empagliflozin attenuates inflammation and myocardial injury in a murine model of sepsis

Objective: This study aimed to evaluate the cardioprotective and anti-inflammatory effects of Empagliflozin in a murine model of polymicrobial sepsis induced by caecal ligation and puncture (CLP). Methods: Thirty-five male Swiss albino mice were randomly assigned into five groups (n = 7): control, sham, sepsis, vehicle (DMSO), and Empagliflozin (10 mg/kg/day for 3 days, intraperitoneally). Sepsis was induced via CLP. Blood and cardiac tissues were collected 24 hours post-CLP for analysis. Serum cardiac troponin I (cTn-I) and tissue levels of NF-κB, TNF-α, and FoxO3 were measured using ELISA. Histopathological evaluation of cardiac tissues was conducted and scored using a standardised injury scale. Results: The sepsis and vehicle groups showed significantly elevated levels of cTn-I (4.13 ± 0.32 ng/mL and 4.08 ± 0.29 ng/mL), NF-κB, TNF-α, and FoxO3 compared to the control and sham groups (all p < 0.01). Empagliflozin treatment significantly reduced these markers (cTn-I: 2.15 ± 0.22 ng/mL; p = 0.012 vs. sepsis). Histologically, Empagliflozin-treated hearts showed reduced myocardial damage (score: 1.14 ± 0.18) compared to the sepsis (3.14 ± 0.26) and vehicle (3.00 ± 0.24) groups. Conclusion: Empagliflozin attenuated cardiac inflammation and injury in a mouse model of sepsis. These preclinical findings support further mechanistic research and warrant clinical investigation of Empagliflozin as a potential adjunctive therapy in septic cardiomyopathy.