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The aim of the present study was to investigate the protective mechanisms and identify the effects of isoquercetin on myocardial infarction in a rat model of acute myocardial infarction (AMI). Isoquercetin ameliorated myocardial infarct size, creatine kinase (CK), CK‑MB and lactic dehydrogenase activity and inhibited inflammation, oxidative stress and heart cell apoptosis in a rat with AMI. Isoquercetin increased endothelial nitric oxide synthase, reduced inducible nitric oxide synthase levels and suppressed the Toll-like receptor 4‑nuclear factor (TLR4‑NF)‑κB signaling pathway in a rat with AMI. Overall, isoquercetin ameliorated AMI through anti‑inflammatory and anti‑apoptotic factors, and regulation of the TLR4‑NF‑κB signaling pathway. Isoquercetin may therefore potentially exert a protective effect against AMI or other heart diseases.

Isoquercetin ameliorates myocardial infarction through anti-inflammation and anti-apoptosis factor and regulating TLR4-NF-κB signal pathway