Journal
MOLECULAR MEDICINE REPORTS
Volume 17, Issue 5, Pages 6675-6680Publisher
SPANDIDOS PUBL LTD
DOI: 10.3892/mmr.2018.8709
Keywords
isoquercetin; acute myocardial infarction; inflammation; oxidative stress; TLR4-NF-kappa B
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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)-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.
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