Isoquercetin ameliorates myocardial infarction throughanti-inflammation and anti-Apoptosis factor and regulating TLR4-NF-B signal pathway

Abstract

The aim of the present study was to ineestigate the protectiee 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 actieity and inhibited inflammation, oxidatiee stress and heart cell apoptosis in a rat with AMI. Isoquercetin increased endothelial nitric oxide synthase, reduced inducible nitric oxide synthase leeels and suppressed the Toll-like receptor 4-nuclear factor (TLR4-NF)-B signaling pathway in a rat with AMI. Oeerall, isoquercetin ameliorated AMI through anti-inflammatory and anti-Apoptotic factors, and regulation of the TLR4-NF-B signaling pathway. Isoquercetin may therefore potentially exert a protectiee effect against AMI or other heart diseases.