Quercetin Reduces Inflammatory Responses in LPS-Stimulated Cardiomyoblasts

Flavonoids possess several biological and pharmacological activities. Quercetin (Q), a naturally occurring flavonoid, has been shown to downregulate inflammatory responses and provide cardioprotection. However, the mechanisms behind the anti-inflammatory properties of Q in cardiac cells are poorly u...

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Main Authors:	Angeloni, Cristina, Hrelia, Silvana
Format:	Online
Language:	English
Published:	Hindawi Publishing Corporation 2012
Online Access:	https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3364695/

id	pubmed-3364695
recordtype	oai_dc
spelling	pubmed-33646952012-06-08 Quercetin Reduces Inflammatory Responses in LPS-Stimulated Cardiomyoblasts Angeloni, Cristina Hrelia, Silvana Research Article Flavonoids possess several biological and pharmacological activities. Quercetin (Q), a naturally occurring flavonoid, has been shown to downregulate inflammatory responses and provide cardioprotection. However, the mechanisms behind the anti-inflammatory properties of Q in cardiac cells are poorly understood. In inflammation, nitric oxide (NO) acts as a proinflammatory mediator and is synthesized by inducible nitric oxide synthase (iNOS) in response to pro-inflammatory agents such as lipopolysaccharide (LPS), a causative agent in myocardial depression during sepsis. In the present study, we evaluated the protective effect of Q on rat cardiac dysfunction during sepsis induced by LPS. Pretreatment of H9c2 cardiomyoblasts with Q inhibited LPS-induced iNOS expression and NO production and counteracted oxidative stress caused by the unregulated NO production that leads to the generation of peroxynitrite and other reactive nitrogen species. In addition, Q pretreatment significantly counteracted apoptosis cell death as measured by immunoblotting of the cleaved caspase 3 and caspase 3 activity. Q also inhibited the LPS-induced phosphorylation of the stress-activated protein kinases (JNK/SAPK) and p38 MAP kinase that are involved in the inhibition of cell growth as well as the induction of apoptosis. In conclusion, these results suggest that Q might serve as a valuable protective agent in cardiovascular inflammatory diseases. Hindawi Publishing Corporation 2012 2012-05-22 /pmc/articles/PMC3364695/ /pubmed/22685622 http://dx.doi.org/10.1155/2012/837104 Text en Copyright © 2012 C. Angeloni and S. Hrelia. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
repository_type	Open Access Journal
institution_category	Foreign Institution
institution	US National Center for Biotechnology Information
building	NCBI PubMed
collection	Online Access
language	English
format	Online
author	Angeloni, Cristina Hrelia, Silvana
spellingShingle	Angeloni, Cristina Hrelia, Silvana Quercetin Reduces Inflammatory Responses in LPS-Stimulated Cardiomyoblasts
author_facet	Angeloni, Cristina Hrelia, Silvana
author_sort	Angeloni, Cristina
title	Quercetin Reduces Inflammatory Responses in LPS-Stimulated Cardiomyoblasts
title_short	Quercetin Reduces Inflammatory Responses in LPS-Stimulated Cardiomyoblasts
title_full	Quercetin Reduces Inflammatory Responses in LPS-Stimulated Cardiomyoblasts
title_fullStr	Quercetin Reduces Inflammatory Responses in LPS-Stimulated Cardiomyoblasts
title_full_unstemmed	Quercetin Reduces Inflammatory Responses in LPS-Stimulated Cardiomyoblasts
title_sort	quercetin reduces inflammatory responses in lps-stimulated cardiomyoblasts
description	Flavonoids possess several biological and pharmacological activities. Quercetin (Q), a naturally occurring flavonoid, has been shown to downregulate inflammatory responses and provide cardioprotection. However, the mechanisms behind the anti-inflammatory properties of Q in cardiac cells are poorly understood. In inflammation, nitric oxide (NO) acts as a proinflammatory mediator and is synthesized by inducible nitric oxide synthase (iNOS) in response to pro-inflammatory agents such as lipopolysaccharide (LPS), a causative agent in myocardial depression during sepsis. In the present study, we evaluated the protective effect of Q on rat cardiac dysfunction during sepsis induced by LPS. Pretreatment of H9c2 cardiomyoblasts with Q inhibited LPS-induced iNOS expression and NO production and counteracted oxidative stress caused by the unregulated NO production that leads to the generation of peroxynitrite and other reactive nitrogen species. In addition, Q pretreatment significantly counteracted apoptosis cell death as measured by immunoblotting of the cleaved caspase 3 and caspase 3 activity. Q also inhibited the LPS-induced phosphorylation of the stress-activated protein kinases (JNK/SAPK) and p38 MAP kinase that are involved in the inhibition of cell growth as well as the induction of apoptosis. In conclusion, these results suggest that Q might serve as a valuable protective agent in cardiovascular inflammatory diseases.
publisher	Hindawi Publishing Corporation
publishDate	2012
url	https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3364695/
_version_	1611533991148519424

Quercetin Reduces Inflammatory Responses in LPS-Stimulated Cardiomyoblasts

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