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Quercetin inhibits lipopolysaccharide-induced nitric oxide production in BV2 microglial cells by suppressing the NF-kappa B pathway and activating the Nrf2-dependent HO-1 pathway

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dc.contributor.authorKang, Chang-Hee-
dc.contributor.authorChoi, Yung Hyun-
dc.contributor.authorMoon, Sung-Kwon-
dc.contributor.authorKim, Wun-Jae-
dc.contributor.authorKim, Gi-Young-
dc.date.available2019-03-09T01:00:53Z-
dc.date.issued2013-11-
dc.identifier.issn1567-5769-
dc.identifier.issn1878-1705-
dc.identifier.urihttps://scholarworks.bwise.kr/cau/handle/2019.sw.cau/14181-
dc.description.abstractAbnormal nitrosative stress-induced neuroinflammation is implicated in the pathogenesis of neurodegenerative diseases. Therefore, it has been thought that nitric oxide (NO) production is a good therapeutic target. In this sense, quercetin is a good chemopreventive component, because it has free radical-scavenging and anti-inflammatory activities. However, explicit mechanisms are not clear in the lipopolysaccharide (LPS)-stimulated BV2 microglial cell line. Here, we found that quercetin significantly suppressed LPS-induced NO production and inducible NO synthase (iNOS) expression. Notably, quercetin inhibited nuclear factor-kappa B (NF-kappa B) activation by inhibiting degradation of the inhibitor of kappa B alpha (I kappa B alpha) in LPS-stimulated BV2 microglial cells corresponding to the inhibitory effect of specific NF-kappa B inhibitors, namely proteasome inhibitor I (PSI) and MG132. Quercetin caused significant increases in the levels of heme oxgenase-1 (HO-1) mRNA and protein. Notably, treatment with an HO-1 inducer, cobalt protoporphyrin (CoPP), significantly diminished LPS-stimulated NO production. Additionally, quercetin induced the specific DNA-binding activity of nuclear factor-2-erythroid 2-related factor 2 (Nrf2), and siRNA-mediated knockdown of Nrf2 expression reduced the inhibitory effect of quercetin on LPS-stimulated NO production by inhibiting HO-1 expression, indicating that quercetin regulated NO production by inducing Nrf2-mediated HO-1 expression. Therefore, quercetin has the potential to decrease nitrosative stress by suppressing NF-kappa B activation and inducing Nrf2-mediated HO-1 expression. (C) 2013 Elsevier B.V. All rights reserved.-
dc.format.extent6-
dc.language영어-
dc.language.isoENG-
dc.publisherELSEVIER SCIENCE BV-
dc.titleQuercetin inhibits lipopolysaccharide-induced nitric oxide production in BV2 microglial cells by suppressing the NF-kappa B pathway and activating the Nrf2-dependent HO-1 pathway-
dc.typeArticle-
dc.identifier.doi10.1016/j.intimp.2013.09.009-
dc.identifier.bibliographicCitationINTERNATIONAL IMMUNOPHARMACOLOGY, v.17, no.3, pp 808 - 813-
dc.description.isOpenAccessN-
dc.identifier.wosid000327280100044-
dc.identifier.scopusid2-s2.0-84884921233-
dc.citation.endPage813-
dc.citation.number3-
dc.citation.startPage808-
dc.citation.titleINTERNATIONAL IMMUNOPHARMACOLOGY-
dc.citation.volume17-
dc.type.docTypeArticle-
dc.publisher.location네델란드-
dc.subject.keywordAuthorQuercetin-
dc.subject.keywordAuthorNitric oxide-
dc.subject.keywordAuthorNitric oxide synthase-
dc.subject.keywordAuthorNuclear factor-kappa B-
dc.subject.keywordAuthorHeme oxgenase-1-
dc.subject.keywordAuthorNuclear factor-2-erythroid 2-related factor 2-
dc.subject.keywordPlusHEME OXYGENASE-1 INDUCTION-
dc.subject.keywordPlusOXIDATIVE STRESS-
dc.subject.keywordPlusEX-VIVO-
dc.subject.keywordPlusEXPRESSION-
dc.subject.keywordPlusGENE-
dc.subject.keywordPlusINOS-
dc.subject.keywordPlusAPOPTOSIS-
dc.subject.keywordPlusKINASE-
dc.subject.keywordPlusTRANSCRIPTION-
dc.subject.keywordPlusINVOLVEMENT-
dc.relation.journalResearchAreaImmunology-
dc.relation.journalResearchAreaPharmacology & Pharmacy-
dc.relation.journalWebOfScienceCategoryImmunology-
dc.relation.journalWebOfScienceCategoryPharmacology & Pharmacy-
dc.description.journalRegisteredClasssci-
dc.description.journalRegisteredClassscie-
dc.description.journalRegisteredClassscopus-
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