New Study Reveals Dual Heart and Brain Protection from Diabetes Drug

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PASADENA, Calif. — March 14, 2025 — A new study led by Dr. Robert A. Kloner, Chief Science Officer and Scientific Director of Cardiovascular Research at Huntington Medical Research Institutes (HMRI), demonstrates that the diabetes medication empagliflozin may protect both the heart and brain from ischemic injury.

Published in Scientific Reports, the paper — “Empagliflozin demonstrates neuroprotective and cardioprotective effects by reducing ischemia/reperfusion damage in rat models of ischemic stroke and myocardial infarction” — shows that the drug significantly reduced tissue damage following experimentally induced stroke and heart attack in rat models.

The research team, including Wangde Dai, Rashid Alavi, Jiajun Li, Juan Carreno, Niema M. Pahlevan, and Robert A. Kloner, found that both acute and chronic treatment with empagliflozin led to markedly smaller infarct sizes and less edema in the brain, as well as reduced infarct and no-reflow areas in the heart.

“These preclinical findings suggest that SGLT2 inhibitors like empagliflozin may have therapeutic potential beyond diabetes management — offering protection against ischemic injury to vital organs,” said Dr. Kloner.

The study adds to growing evidence that medications developed for metabolic disease may hold broader promise for cardiovascular and neurological health.

Full article: Scientific Reports, March 14, 2025

Abstract:

Sodium-glucose co-transporter 2 (SGLT2) inhibitors have demonstrated potential neuroprotective and cardioprotective effects in preliminary studies. This study evaluates the efficacy of empagliflozin (EMPA) in reducing ischemia/reperfusion damage in both the brain and heart using rat models. Ischemic stroke and myocardial infarction (MI) were induced in male Sprague-Dawley rats, which were randomized into three groups: (1) Control (no EMPA), (2) Acute treatment (EMPA, 10 mg/kg IV, administered 10 min before ischemia and 1 min before reperfusion), and (3) Chronic treatment (EMPA, 20 mg/kg in food for 7 days before ischemia). Stroke was induced by middle cerebral artery occlusion (MCAO) for one hour, followed by 3 h of reperfusion, and MI was induced by left coronary artery occlusion for 30 min, followed by 3 h of reperfusion. Brain and heart tissues were analyzed for anatomic size of myocardial infarction and stroke. In the brain, cerebral infarction was significantly smaller in both EMPA treatment groups compared to controls (acute: 3.7 ± 1.2%, chronic: 6.9 ± 2.1% vs. control: 14.5 ± 2.5%, p < 0.05). Edema was also reduced in the EMPA groups (acute: 5.5 ± 0.9%, chronic: 5.9 ± 0.8% vs. control: 9.6 ± 1.2%, p < 0.05). In the heart, MI size was significantly reduced in both EMPA groups (acute: 46.9 ± 2.0%, chronic: 48.8 ± 5.8% vs. control: 70.0 ± 2.6%, p < 0.05), and no-reflow size was smaller in the EMPA groups (acute: 36.3 ± 3.3%, chronic: 33.9 ± 4.3% vs. control: 53.4 ± 3.3%, p < 0.05). EMPA treatment, both acute and chronic, significantly reduces cerebral infarct volume and edema, as well as myocardial infarct size and no-reflow in rat models of ischemic stroke and myocardial ischemia/reperfusion, indicating substantial neuroprotective and cardioprotective effects.