Isoquercetin ameliorates myocardial infarction through anti-inflammation and anti-apoptosis factor and regulating TLR4-NF-[kappa]B signal pathway

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)-[kappa]B signaling pathway in a rat with AMI. Overall, isoquercetin ameliorated AMI through anti-inflammatory and anti-apoptotic factors, and regulation of the TLR4-NF-[kappa]B signaling pathway. Isoquercetin may therefore potentially exert a protective effect against AMI or other heart diseases. Key words: isoquercetin, acute myocardial infarction, inflammation, oxidative stress, TLR4-NF-[kappa]B