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Cardamonin Inhibits the Expression of Inducible Nitric Oxide Synthase Induced by TLR2, 4, and 6 Agonists

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dc.contributor.author김아연-
dc.contributor.author심현진-
dc.contributor.author김수연-
dc.contributor.author허성혜-
dc.contributor.author윤형선-
dc.date.accessioned2021-08-11T13:24:00Z-
dc.date.available2021-08-11T13:24:00Z-
dc.date.created2021-06-17-
dc.date.issued2018-
dc.identifier.urihttps://scholarworks.bwise.kr/sch/handle/2021.sw.sch/6657-
dc.description.abstractToll-like receptors (TLRs) play an important role for host defense against invading pathogens. The activation of TLRs signaling leads to the activation of NF-κB and the expression of pro-inflammatory gene products such as cytokines and inducible nitric oxide synthase (iNOS). To evaluate the therapeutic potential of cardamonin, which is a naturally occurring chalcone from Alpinia species (zingiberaceous plant species), NF-κB activation and iNOS expression induced by MALP-2 (TLR2 and TLR6 agonist) or LPS (TLR4 agonist) were examined. Cardamonin inhibited the activation of NF-κB induced by MALP-2 or LPS. Cardamonin also suppressed the iNOS expression induced by MALP-2 or LPS. These results suggest that cardamonin has the specific mechanism for anti-inflammatory responses by regulating of TLRs signaling pathway.-
dc.language한국어-
dc.language.isoko-
dc.publisher대한의생명과학회-
dc.titleCardamonin Inhibits the Expression of Inducible Nitric Oxide Synthase Induced by TLR2, 4, and 6 Agonists-
dc.title.alternativeCardamonin Inhibits the Expression of Inducible Nitric Oxide Synthase Induced by TLR2, 4, and 6 Agonists-
dc.typeArticle-
dc.contributor.affiliatedAuthor윤형선-
dc.identifier.doi10.15616/BSL.2018.24.2.102-
dc.identifier.bibliographicCitation대한의생명과학회지, v.24, no.2, pp.102 - 107-
dc.relation.isPartOf대한의생명과학회지-
dc.citation.title대한의생명과학회지-
dc.citation.volume24-
dc.citation.number2-
dc.citation.startPage102-
dc.citation.endPage107-
dc.type.rimsART-
dc.identifier.kciidART002364760-
dc.description.journalClass3-
dc.subject.keywordAuthorCardamonin-
dc.subject.keywordAuthorInducible nitric oxide synthase-
dc.subject.keywordAuthorTLR-
dc.subject.keywordAuthorInflammation-
dc.subject.keywordAuthorLPS-
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