Blockade of nuclear factor-κB signaling pathway and anti-inflammatory activity of cardamomin, a chalcone analog from Alpinia conchigera

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dc.contributor.authorJeong-Hyung Lee-
dc.contributor.authorHaeng Sun Jung-
dc.contributor.authorP M Giang-
dc.contributor.authorX Jin-
dc.contributor.authorSangku Lee-
dc.contributor.authorP T Son-
dc.contributor.authorDongho Lee-
dc.contributor.authorYoung-Soo Hong-
dc.contributor.authorKyeong Lee-
dc.contributor.authorJung Joon Lee-
dc.date.accessioned2017-04-19T09:04:00Z-
dc.date.available2017-04-19T09:04:00Z-
dc.date.issued2006-
dc.identifier.issn0022-3565-
dc.identifier.uri10.1124/jpet.105.092486ko
dc.identifier.urihttps://oak.kribb.re.kr/handle/201005/7259-
dc.description.abstractNuclear factor-κB (NF-κB) and the signaling pathways that regulate its activity have become a focal point for intense drug discovery and development efforts. NF-κB regulates the transcription of a large number of genes, particularly those involved in immune, inflammatory, and antiapoptotic responses. In our search for NF-κB inhibitors from natural resources, we identified cardamomin, 2′,4′-dihydroxy-6′-methoxychalcone, as an inhibitor of NF-κB activation from Alpinia conchigera Griff (Zingiberaceae). In present study, we demonstrated the effect of cardamomin on NF-κB activation in lipopolysaccharide (LPS)-stimulated RAW264.7 cells and LPS-induced mortality. This compound significantly inhibited the induced expression of NF-κB reporter gene by LPS or tumor necrosis factor (TNF)-α in a dose-dependent manner. LPS-induced production of TNF-α and NO as well as expression of inducible nitric-oxide synthase and cyclooxygenase-2 was significantly suppressed by the treatment of cardamomin in RAW264.7 cells. Also, cardamomin inhibited not only LPS-induced degradation and phosphorylation of inhibitor κBα (IκBα) but also activation of inhibitor κB (IκB) kinases and nuclear translocation of NF-κB. Further analyses revealed that cardamomin did not directly inhibit IκB kinases, but it significantly suppressed LPS-induced activation of Akt. Moreover, cardamomin suppressed transcriptional activity and phosphorylation of Ser536 of RelA/p65 subunit of NF-κB. However, this compound did not inhibit LPS-induced activation of extracellular signal-regulated kinase and stress-activated protein kinase/c-Jun NH 2-terminal kinase, but significantly impaired activation of p38 mitogen-activated protein kinase. We also demonstrated that pretreatment of cardamomin rescued C57BL/6 mice from LPS-induced mortality in conjunction with decreased serum level of TNF-α. Together, cardamomin could be valuable candidate for the intervention of NF-κB-dependent pathological condition such as inflammation.-
dc.publisherAmer Soc Pharmacology Experimental Therapeutics-
dc.titleBlockade of nuclear factor-κB signaling pathway and anti-inflammatory activity of cardamomin, a chalcone analog from Alpinia conchigera-
dc.title.alternativeBlockade of nuclear factor-κB signaling pathway and anti-inflammatory activity of cardamomin, a chalcone analog from Alpinia conchigera-
dc.typeArticle-
dc.citation.titleJournal of Pharmacology and Experimental Therapeutics-
dc.citation.number1-
dc.citation.endPage278-
dc.citation.startPage271-
dc.citation.volume316-
dc.contributor.affiliatedAuthorJeong-Hyung Lee-
dc.contributor.affiliatedAuthorHaeng Sun Jung-
dc.contributor.affiliatedAuthorSangku Lee-
dc.contributor.affiliatedAuthorDongho Lee-
dc.contributor.affiliatedAuthorYoung-Soo Hong-
dc.contributor.affiliatedAuthorKyeong Lee-
dc.contributor.affiliatedAuthorJung Joon Lee-
dc.contributor.alternativeName이정형-
dc.contributor.alternativeName정행선-
dc.contributor.alternativeNameGiang-
dc.contributor.alternativeNameJin-
dc.contributor.alternativeName이상구-
dc.contributor.alternativeNameSon-
dc.contributor.alternativeName이동호-
dc.contributor.alternativeName홍영수-
dc.contributor.alternativeName이경-
dc.contributor.alternativeName이정준-
dc.identifier.bibliographicCitationJournal of Pharmacology and Experimental Therapeutics, vol. 316, no. 1, pp. 271-278-
dc.identifier.doi10.1124/jpet.105.092486-
dc.description.journalClassY-
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Ochang Branch Institute > Chemical Biology Research Center > 1. Journal Articles
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