Arvelexin from Brassica rapa suppresses NF-κB-regulated pro-inflammatory gene expression by inhibiting activation of IκB kinase

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dc.contributor.authorJ S Shin-
dc.contributor.authorY S Noh-
dc.contributor.authorY S Lee-
dc.contributor.authorY W Cho-
dc.contributor.authorN I Baek-
dc.contributor.authorM S Choi-
dc.contributor.authorTae Sook Jeong-
dc.contributor.authorE Kang-
dc.contributor.authorH G Chung-
dc.contributor.authorK T Lee-
dc.date.accessioned2017-04-19T09:24:47Z-
dc.date.available2017-04-19T09:24:47Z-
dc.date.issued2011-
dc.identifier.issn0007-1188-
dc.identifier.uri10.1111/j.1476-5381.2011.01351.xko
dc.identifier.urihttps://oak.kribb.re.kr/handle/201005/10274-
dc.description.abstractBACKGROUND AND PURPOSE Brassica rapa species constitute one of the major sources of food. In the present study, we investigated the anti-inflammatory effects and the underlying molecular mechanism of arvelexin, isolated from B. rapa, on lipopolysaccharide (LPS)-stimulated RAW264.7 macrophages and on a model of septic shock induced by LPS. EXPERIMENTAL APPROACH The expression of Inducible nitric oxide synthase (iNOS) and COX-2, TNF-α, IL-6 and IL-1β were determined by Western blot and/or RT-PCR respectively. To elucidate the underlying mechanism(s), activation of NF-κB activation and its pathways were investigated by electrophoretic mobility shift assay, reporter gene and Western blot assays. In addition, the in vivo anti-inflammatory effects of arvelexin were evaluated in endotoxaemia induced with LPS. KEY RESULTS Promoter assays for iNOS and COX-2 revealed that arvelexin inhibited LPS-induced NO and prostaglandin E2 production through the suppression of iNOS and COX-2 at the level of gene transcription. In addition, arvelexin inhibited NF-κB-dependent inflammatory responses by modulating a series of intracellular events of IκB kinase (IKK)-inhibitor κBα (IκBα)-NF-κB signalling. Moreover, arvelexin inhibited IKKβ-elicited NF-κB activation as well as iNOS and COX-2 expression. Serum levels of NO and inflammatory cytokines and mortality in mice challenged injected with LPS were significantly reduced by arvelexin. CONCLUSION AND IMPLICATIONS Arvelexin down-regulated inflammatory iNOS, COX-2, TNF-α, IL-6 and IL-1β gene expression in macrophages interfering with the activation of IKKβ and p38 mitogen-activated protein kinase, and thus, preventing NF-κB activation.-
dc.publisherWiley-
dc.titleArvelexin from Brassica rapa suppresses NF-κB-regulated pro-inflammatory gene expression by inhibiting activation of IκB kinase-
dc.title.alternativeArvelexin from Brassica rapa suppresses NF-κB-regulated pro-inflammatory gene expression by inhibiting activation of IκB kinase-
dc.typeArticle-
dc.citation.titleBritish Journal of Pharmacology-
dc.citation.number1-
dc.citation.endPage158-
dc.citation.startPage145-
dc.citation.volume164-
dc.contributor.affiliatedAuthorTae Sook Jeong-
dc.contributor.alternativeName-
dc.contributor.alternativeName-
dc.contributor.alternativeName-
dc.contributor.alternativeName-
dc.contributor.alternativeName백남인-
dc.contributor.alternativeName최명숙-
dc.contributor.alternativeName정태숙-
dc.contributor.alternativeName-
dc.contributor.alternativeName-
dc.contributor.alternativeName-
dc.identifier.bibliographicCitationBritish Journal of Pharmacology, vol. 164, no. 1, pp. 145-158-
dc.identifier.doi10.1111/j.1476-5381.2011.01351.x-
dc.subject.keywordarvelexin-
dc.subject.keywordBrassica rapa-
dc.subject.keywordcyclooxygenase-2-
dc.subject.keywordIKK-
dc.subject.keywordinducible nitric oxide-
dc.subject.keywordinflammation-
dc.subject.keywordNF-κB-
dc.subject.keywordpaw oedema-
dc.subject.localarvelexin-
dc.subject.localBrassica rapa-
dc.subject.localbrassica rapa-
dc.subject.localCyclooxygenase 2-
dc.subject.localCyclooxygenase-2-
dc.subject.localCyclooxygenase-2 (COX-2)-
dc.subject.localcyclooxygenase-2-
dc.subject.localIKK-
dc.subject.localinducible nitric oxide-
dc.subject.localInflammation-
dc.subject.localinflammation-
dc.subject.localnflammation-
dc.subject.localNFkappaB-
dc.subject.localNFκB-
dc.subject.localNf-κB-
dc.subject.localNf-κb-
dc.subject.localNuclear factor (NF)-κB-
dc.subject.localNuclear factor kappa B-
dc.subject.localNuclear factor kappaB-
dc.subject.localNuclear factor κB-
dc.subject.localNuclear factor κB (NF-κB)-
dc.subject.localNuclear factor-kappa B-
dc.subject.localNuclear factor-kappa B (NF-κB)-
dc.subject.localNuclear factor-kappaB-
dc.subject.localNuclear factor-κB-
dc.subject.localNuclear factor-κb-
dc.subject.localNF-kB-
dc.subject.localNF-kappa B-
dc.subject.localNF-kappaB-
dc.subject.localNF-ΚB-
dc.subject.localNF-κ B-
dc.subject.localNF-κB-
dc.subject.localNF-κB (nuclear factor kappa-B)-
dc.subject.localnuclear factor kappa B-
dc.subject.localnuclear factor κB-
dc.subject.localnuclear factor-kappaB-
dc.subject.localnuclear factor-kappaB (NF-κB)-
dc.subject.localnuclear factor-κB-
dc.subject.localnuclear factorκB-
dc.subject.localpaw oedema-
dc.description.journalClassY-
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Division of Biomedical Research > Microbiome Convergence Research Center > 1. Journal Articles
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