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dc.contributor.author김희선-
dc.contributor.author김한수-
dc.date.accessioned2018-12-07T16:30:18Z-
dc.date.available2018-12-07T16:30:18Z-
dc.date.issued2017-
dc.identifier.issn1976-9148-
dc.identifier.otherOAK-21579-
dc.identifier.urihttp://dspace.ewha.ac.kr/handle/2015.oak/247266-
dc.description.abstractGalangin (3,5,7-trihydroxyflavone) is a polyphenolic compound abundant in honey and medicinal herbs, such as Alpinia officinarum. In this study, we investigated the anti-inflammatory effects of galangin under in vitro and in vivo neuroinflammatory conditions caused by polyinosinic-polycytidylic acid (poly(I:C)), a viral mimic dsRNA analog. Galangin suppressed the production of nitric oxide, reactive oxygen species, and pro-inflammatory cytokines in poly(I:C)-stimulated BV2 microglia. On the other hand, galangin enhanced anti-inflammatory interleukin (IL)-10 production. Galangin also suppressed the expression of pro-inflammatory markers in poly(I:C)-injected mouse brains. Further mechanistic studies showed that galangin inhibited poly(I:C)-induced nuclear factor (NF)-κB activity and phosphorylation of Akt without affecting MAP kinases. Interestingly, galangin increased the expression and transcriptional activity of peroxisome proliferator-activated receptor (PPAR)-γ, known to play an anti-inflammatory role. To investigate whether PPAR-γ is involved in the anti-inflammatory function of galangin, BV2 cells were pre-treated with PPAR-γ antagonist before treatment of galangin. We found that PPAR-γ antagonist significantly blocked galangin-mediated upregulation of IL-10 and attenuated the inhibition of tumor necrosis factor (TNF)-α and IL-6 in poly(I:C)-stimulated microglia. In conclusion, our data suggest that PI3K/Akt, NF-κB, and PPAR-γ play a pivotal role in mediating the anti-inflammatory effects of galangin in poly(I:C)-stimulated microglia. © 2017 The Korean Society of Applied Pharmacology.-
dc.description.sponsorshipMinistry of Science, ICT and Future Planning-
dc.languageEnglish-
dc.publisherKorean Society of Applied Pharmacology-
dc.subjectGalangin-
dc.subjectMicroglia-
dc.subjectNF-κB-
dc.subjectPI3K/Akt-
dc.subjectPoly(I:C)-
dc.subjectPPAR-γ signaling-
dc.titleGalangin suppresses pro-inflammatory gene expression in polyinosinic-polycytidylic acid-stimulated microglial cells-
dc.typeArticle-
dc.relation.issue6-
dc.relation.volume25-
dc.relation.indexSCIE-
dc.relation.indexSCOPUS-
dc.relation.indexKCI-
dc.relation.startpage641-
dc.relation.lastpage647-
dc.relation.journaltitleBiomolecules and Therapeutics-
dc.identifier.doi10.4062/biomolther.2017.173-
dc.identifier.wosidWOS:000415274600011-
dc.identifier.scopusid2-s2.0-85033606834-
dc.author.googleChoi M.-J.-
dc.author.googlePark J.-S.-
dc.author.googlePark J.-E.-
dc.author.googleKim H.S.-
dc.author.googleKim H.-S.-
dc.contributor.scopusid김희선(56431262700)-
dc.contributor.scopusid김한수(56509934900)-
dc.date.modifydate20181207113252-
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의과대학 > 의학과 > Journal papers
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