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dc.contributor.author김원기*
dc.contributor.author김희선*
dc.contributor.author박진선*
dc.date.accessioned2016-08-28T11:08:40Z-
dc.date.available2016-08-28T11:08:40Z-
dc.date.issued2004*
dc.identifier.issn0165-5728*
dc.identifier.otherOAK-2206*
dc.identifier.urihttps://dspace.ewha.ac.kr/handle/2015.oak/219433-
dc.description.abstractIn the present study, we demonstrate that sodium butyrate repressed IFN-γ-induced expression of iNOS and TNF-α, but had little effect on LPS-induced expression in BV2 murine microglial cells. Sodium butyrate significantly inhibited NF-κB binding and NF-κB-mediated transcription induced by IFN-γ, suggesting that the anti-inflammatory effect of sodium butyrate is mediated via specific inhibition of the NF-κB pathway. IFN-γ is a major stimulator of innate and adaptive immune response. Thus, the specific down-regulation of IFN-γ-induced microglial activation by sodium butyrate may provide potential therapeutic strategies for a variety of inflammatory diseases in the central nervous system. © 2004 Elsevier B.V. All rights reserved.*
dc.languageEnglish*
dc.titleSodium butyrate suppresses interferon-gamma-, but not lipopolysaccharide- mediated induction of nitric oxide and tumor necrosis factor-alpha in microglia*
dc.typeArticle*
dc.relation.issue41276*
dc.relation.volume151*
dc.relation.indexSCI*
dc.relation.indexSCIE*
dc.relation.indexSCOPUS*
dc.relation.startpage85*
dc.relation.lastpage93*
dc.relation.journaltitleJournal of Neuroimmunology*
dc.identifier.doi10.1016/j.jneuroim.2004.02.006*
dc.identifier.wosidWOS:000221895000010*
dc.identifier.scopusid2-s2.0-2442549715*
dc.author.googleKim H.-S.*
dc.author.googleWhang S.-Y.*
dc.author.googleWoo M.-S.*
dc.author.googlePark J.-S.*
dc.author.googleKim W.-K.*
dc.author.googleHan I.-O.*
dc.contributor.scopusid김원기(34770946200)*
dc.contributor.scopusid김희선(57191372551)*
dc.contributor.scopusid박진선(54914743600)*
dc.date.modifydate20240215165648*
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자연과학대학 > 화학·나노과학전공 > Journal papers
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