Empagliflozin prevents from early cardiac injury post myocardial infarction in non-diabetic mice

Objectives: Sodium-glucose cotransporter 2 (SGLT2) inhibitors have been confirmed to reduce the rate of rehospitalization for heart failure and cardiovascular death in diabetic patients. The aim of our study was to investigate the cardioprotective role of SGLT2 inhibitors in early myocardial infarction (MI) of non-diabetic mice. Methods: C57BL/6 mice underwent left artery coronary artery descending (LAD) ligation to induce MI. Following the surgery, animals were randomized to receive saline or empagliflozin. Empagliflozin (EMPA) was administrated at 10 mg/kg per day by oral gavage for 2 weeks. Echocardiography, histological staining and qualitative RT-PCR were performed to assess the cardiac remodeling post MI. In vitro experiments were performed to evaluate the effect of empagliflozin on apoptosis, oxidative stress and mitochondrial membrane potential of cardiomyocyte subjected to hypoxic treatment. Results: Compared with MI group, the empagliflozin treatment group showed improved cardiac function, reduced infarct size and interstitial fibrosis. Empagliflozin also inhibited cardiomyocyte apoptosis by alleviating oxidative stress and restoring mitochondrial membrane potential. Immunoblotting analysis revealed activated AMPactivated protein kinase (AMPK) signaling may mediated the cardioprotective role of empagliflozin. Conclusions: In summary, empagliflozin could inhibit cardiomyocyte apoptosis and improve cardiac remodeling early MI, which provided insights into the benefic effect of empagliflozin on MI patients without diabetes.

Automated summary

The study demonstrated that the SGLT2 inhibitor empagliflozin could improve cardiac remodeling in early myocardial infarction of non-diabetic mice by reducing cardiomyocyte apoptosis, oxidative stress, and restoring mitochondrial membrane potential. The activation of AMP-activated protein kinase (AMPK) signaling pathway may mediate the cardioprotective role of empagliflozin.