What question did this study set out to answer?

This study aims to evaluate empagliflozin's potential to protect the heart from doxorubicin-induced damage.

April 1, 2026Open Access

Empagliflozin Mitigates Doxorubicin-Induced Cardiotoxicity in Rats: Electrocardiographic, Biochemical, and Histopathological Evidence

Resultado clave

Empagliflozin significantly mitigated doxorubicin-induced cardiotoxicity in rats by attenuating ECG abnormalities, lowering troponin elevation, and reducing structural myocardial damage.

Puntos clave

This study aims to evaluate empagliflozin's potential to protect the heart from doxorubicin-induced damage.
Thirty healthy adult rats were randomized into five groups.
Empagliflozin was administered orally at 10 mg/kg/day with or without doxorubicin.
Cumulative doxorubicin exposure of 15 mg/kg was used to induce cardiotoxicity.
Serial electrocardiograms were recorded and histopathological analysis was performed.
Doxorubicin exposure led to significant QT/QTc prolongation and troponin elevation.
Histological examination showed cardiomyocyte vacuolization and increased fibrosis in the doxorubicin group.
Empagliflozin administration reduced ECG abnormalities and myocardial damage.

PICO estructurado

Does empagliflozin prevent doxorubicin-induced cardiotoxicity in rats?

Población

Healthy adult rats

Intervención

Empagliflozin 10 mg/kg/day orally, administered either concomitantly with doxorubicin or as a 14-day preconditioning course

Comparador

Doxorubicin alone and healthy controls

Resultado

Cardiotoxicity assessed by electrocardiographic changes, biochemical markers (troponin), and histopathological lesionssurrogate

Empagliflozin demonstrates significant cardioprotective effects against doxorubicin-induced cardiotoxicity in a preclinical rat model, supporting further investigation of SGLT2 inhibitors in cardio-oncology.

Resultado numérico

Tasa de eventos absoluta: 0% vs 0%

Resumen

Doxorubicin (DOX) is a widely used anthracycline, but its clinical use is limited by dose-dependent cardiotoxicity. This experimental study evaluated the cardioprotective potential of empagliflozin (EMPA) against DOX-induced cardiotoxicity. Thirty healthy adult rats were randomized into five groups (n = 6): control (group I), EMPA (group II), EMPA + DOX (group III), DOX (group IV), and EMPA-preconditioning + DOX (group V). EMPA was administered orally at 10 mg/kg/day, either concomitantly with DOX or as a 14-day preconditioning course. Cumulative DOX exposure reached 15 mg/kg to establish a reproducible cardiotoxicity model. Serial electrocardiograms (ECGs) were recorded, blood samples were collected, and hearts were harvested for detailed histopathological analysis. Compared with the control group, group IV demonstrated significant QT/QTc prolongation and repolarization abnormalities, marked troponin elevation, and characteristic histological lesions, including cardiomyocyte vacuolization, loss of striations, diffuse inflammation, myocyte atrophy, and increased fibrosis. In groups receiving EMPA with DOX exposure (groups III and V), ECG changes were attenuated, troponin elevation was lower, and structural myocardial damage was substantially reduced, with better preservation of cardiomyocyte architecture and less fibrosis. These results suggest that EMPA provides significant cardioprotection against DOX-induced cardiotoxicity in rats, supporting further investigation of SGLT2 inhibitors in cardio-oncology.

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