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Cited 35 time in webofscience Cited 39 time in scopus
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Corosolic acid ameliorates acute inflammation through inhibition of IRAK-1 phosphorylation in macrophages

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dc.contributor.authorKim, Seung-Jae-
dc.contributor.authorCha, Ji-Young-
dc.contributor.authorKang, Hye Suk-
dc.contributor.authorLee, Jae-Ho-
dc.contributor.authorLee, Ji Yoon-
dc.contributor.authorPark, Jae-Hyung-
dc.contributor.authorBae, Jae-Hoon-
dc.contributor.authorSong, Dae-Kyu-
dc.contributor.authorIm, Seung-Soon-
dc.date.available2020-02-28T06:44:09Z-
dc.date.created2020-02-06-
dc.date.issued2016-
dc.identifier.issn1976-6696-
dc.identifier.urihttps://scholarworks.bwise.kr/gachon/handle/2020.sw.gachon/9753-
dc.description.abstractCorosolic acid (CA), a triterpenoid compound isolated from Lagerstroemia speciosa L. (Banaba) leaves, exerts anti-inflammatory effects by regulating phosphorylation of interleukin receptor-associated kinase (IRAK)-2 via the NF-kappa B cascade. However, the protective effect of CA against endotoxic shock has not been reported. LPS (200 ng/mL, 30 min) induced phosphorylation of IRAK-1 and treatment with CA (10 mu M) significantly attenuated this effect. In addition, CA also reduced protein levels of NLRP3 and ASC which are the main components of the inflammasome in BMDMs. LPS-induced inflammasome assembly through activation of IRAK-1 was down-regulated by CA challenge. Treatment with Bay11-7082, an inhibitor of I kappa B-alpha, had no effect on CA-mediated inhibition of IRAK-1 activation, indicating that CA-mediated attenuation of IRAK-1 phosphorylation was independent of NF-kappa B signaling. These results demonstrate that CA ameliorates acute inflammation in mouse BMDMs and CA may be useful as a pharmacological agent to prevent acute inflammation.-
dc.language영어-
dc.language.isoen-
dc.publisherKOREAN SOCIETY BIOCHEMISTRY & MOLECULAR BIOLOGY-
dc.relation.isPartOfBMB REPORTS-
dc.subjectTOLL-LIKE RECEPTORS-
dc.subjectNF-KAPPA-B-
dc.subjectINTERLEUKIN-1 RECEPTOR-
dc.subjectNLRP3 INFLAMMASOME-
dc.subjectINNATE IMMUNITY-
dc.subjectKINASE-
dc.subjectCANCER-
dc.subjectACTIVATION-
dc.subjectEXPRESSION-
dc.subjectDISEASE-
dc.titleCorosolic acid ameliorates acute inflammation through inhibition of IRAK-1 phosphorylation in macrophages-
dc.typeArticle-
dc.type.rimsART-
dc.description.journalClass1-
dc.identifier.wosid000383786500007-
dc.identifier.doi10.5483/BMBRep.2016.49.5.241-
dc.identifier.bibliographicCitationBMB REPORTS, v.49, no.5, pp.276 - 281-
dc.identifier.kciidART002109539-
dc.identifier.scopusid2-s2.0-84970038542-
dc.citation.endPage281-
dc.citation.startPage276-
dc.citation.titleBMB REPORTS-
dc.citation.volume49-
dc.citation.number5-
dc.contributor.affiliatedAuthorCha, Ji-Young-
dc.type.docTypeArticle-
dc.subject.keywordAuthorAcute inflammation-
dc.subject.keywordAuthorCorosolic acid-
dc.subject.keywordAuthorInflammasome-
dc.subject.keywordAuthorIRAK-1-
dc.subject.keywordAuthorMacrophages-
dc.subject.keywordPlusTOLL-LIKE RECEPTORS-
dc.subject.keywordPlusNF-KAPPA-B-
dc.subject.keywordPlusINTERLEUKIN-1 RECEPTOR-
dc.subject.keywordPlusNLRP3 INFLAMMASOME-
dc.subject.keywordPlusINNATE IMMUNITY-
dc.subject.keywordPlusKINASE-
dc.subject.keywordPlusCANCER-
dc.subject.keywordPlusACTIVATION-
dc.subject.keywordPlusEXPRESSION-
dc.subject.keywordPlusDISEASE-
dc.relation.journalResearchAreaBiochemistry & Molecular Biology-
dc.relation.journalWebOfScienceCategoryBiochemistry & Molecular Biology-
dc.description.journalRegisteredClassscie-
dc.description.journalRegisteredClassscopus-
dc.description.journalRegisteredClasskci-
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