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Anti-inflammatory effect of quercetin and galangin in LPS-stimulated RAW264.7 macrophages and DNCB-induced atopic dermatitis animal models

DC Field Value Language
dc.contributor.authorLe, Hae Nim-
dc.contributor.authorShin, Seong Ah-
dc.contributor.authorChoo, Gang Sik-
dc.contributor.authorKim, Hyeong Jin-
dc.contributor.authorPark, Young Seok-
dc.contributor.authorKim, Byeong Soo-
dc.contributor.authorKim, Sang Ki-
dc.contributor.authorCho, Sung Dae-
dc.contributor.authorNam, Jeong Seok-
dc.contributor.authorChoi, Chang Sun-
dc.contributor.authorChe, Jeong Hwan-
dc.contributor.authorPark, Byung Kwon-
dc.contributor.authorJung, Ji Youn-
dc.creator조성대-
dc.date.accessioned2019-04-25T01:21:17Z-
dc.date.available2020-04-05T01:21:17Z-
dc.date.created2019-03-20-
dc.date.issued2018-02-
dc.identifier.citationInternational Journal of Molecular Medicine, Vol.41 No.2, pp.888-898-
dc.identifier.issn1107-3756-
dc.identifier.urihttps://hdl.handle.net/10371/149209-
dc.description.abstractFlavonols are compounds that have been shown to possess potent anti-inflammatory effects in cellular and animal models of inflammation. In the present study, the anti-inflammatory effects and mechanisms of two natural flavonols, quercetin and galangin, in lipopolysaccharide (LPS)-stimulated RAW264.7 macrophages were investigated. It was identified that quercetin and galangin markedly reduced the production of nitric oxide (NO), inducible NO synthase and interleukin-6, and the nuclear translocation of nuclear factor-kappa B (NF-kappa B). In addition, LPS-induced activation of extracellular signal-regulated kinase 1/2 (Erk1/2) and c-Jun N-terminal kinase (JNK) was suppressed by quercetin and galangin. Taken together, these data implied that NF-kappa B, Erk1/2 and JNK may be potential molecular targets of quercetin and galangin in an LPS-induced inflammatory response. Subsequently, the effects of oral administration of quercetin or galangin, either alone or in combination, in a 2,4-dinitrochlorobenzene-induced atopic dermatitis (AD) mouse model were investigated. As a result, measurements of ear thickness and the levels of serum immunoglobulin E, and histological analysis revealed that the two flavonols led to a decrease in inflammation, whereas, in combination, they were even more effective. These results suggested that quercetin and galangin may be promising therapeutic agents for AD. Additionally, their combination may be a novel therapeutic strategy for the prevention of AD.-
dc.language영어-
dc.language.isoenen
dc.publisherDemetrios A. Spandidos Ed. & Pub.-
dc.titleAnti-inflammatory effect of quercetin and galangin in LPS-stimulated RAW264.7 macrophages and DNCB-induced atopic dermatitis animal models-
dc.typeArticle-
dc.identifier.doi10.3892/ijmm.2017.3296-
dc.citation.journaltitleInternational Journal of Molecular Medicine-
dc.identifier.wosid000423222200032-
dc.identifier.scopusid2-s2.0-85040467710-
dc.description.srndOAIID:RECH_ACHV_DSTSH_NO:T201800242-
dc.description.srndRECH_ACHV_FG:RR00200001-
dc.description.srndADJUST_YN:-
dc.description.srndEMP_ID:A080405-
dc.description.srndCITE_RATE:2.784-
dc.description.srndFILENAME:C4_201802_Anti-inflammatory effects of quercetin and galangin in LPS-stimulated macrophages and DNCB-induced atopic dermatitis animal models_International Journal of Molecular Medicine.pdf-
dc.description.srndDEPT_NM:치의과학과-
dc.description.srndEMAIL:efiwdsc@snu.ac.kr-
dc.description.srndSCOPUS_YN:Y-
dc.description.srndFILEURL:https://srnd.snu.ac.kr/eXrepEIR/fws/file/8b463a8b-205e-4eb2-87c0-743183d6ac81/link-
dc.citation.endpage898-
dc.citation.number2-
dc.citation.startpage888-
dc.citation.volume41-
dc.description.isOpenAccessY-
dc.contributor.affiliatedAuthorCho, Sung Dae-
dc.identifier.srndT201800242-
dc.type.docTypeArticle-
dc.description.journalClass1-
dc.subject.keywordPlusNF-KAPPA-B-
dc.subject.keywordPlusRAW 264.7 CELLS-
dc.subject.keywordPlusNITRIC-OXIDE-
dc.subject.keywordPlusINFLAMMATORY DISEASES-
dc.subject.keywordPlusSIGNALING PATHWAYS-
dc.subject.keywordPlusENDOTOXIN-SHOCK-
dc.subject.keywordPlusMAST-CELLS-
dc.subject.keywordPlusTNF-ALPHA-
dc.subject.keywordPlusLIPOPOLYSACCHARIDE-
dc.subject.keywordPlusINHIBITION-
dc.subject.keywordAuthorhydroxy group-
dc.subject.keywordAuthorflavonol-
dc.subject.keywordAuthoranti-inflammation-
dc.subject.keywordAuthornuclear factor-kappa B-
dc.subject.keywordAuthormitogen-activated protein kinase-
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