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dc.contributor.author김원기*
dc.contributor.author김희선*
dc.date.accessioned2016-08-28T11:08:25Z-
dc.date.available2016-08-28T11:08:25Z-
dc.date.issued2004*
dc.identifier.issn0028-3908*
dc.identifier.otherOAK-12806*
dc.identifier.urihttps://dspace.ewha.ac.kr/handle/2015.oak/228877-
dc.description.abstractExcessive proinflammatory cytokine and NO production by activated microglia play a role in neurodegenerative disorders. In this study, we found that a new compound KL-1037 suppressed LPS-induced NO release/inducible nitric oxide synthase expression in BV2 mouse microglial cells. In addition, KL-1037 prominently diminished LPS-induced production of pro-inflammatory cytokines such as TNF-α, IL-1β and IL-6, while it increased anti-inflammatory IL-10 and TGF-β1 production. By RNase protection assay and RT-PCR, we showed that KL-1037 regulated iNOS and cytokines at transcriptional or post-transcriptional level. Further analysis of molecular mechanisms revealed that KL-1037 prominently increased intracellular cAMP levels and potentiated LPS-induced pCREB expression. However, LPS-induced MAP kinase or NF-κB activities were slightly or little changed by KL-1037. Treatment with cAMP antagonist or IL-10 neutralizing antibody completely reversed upregulation of IL-10 and partially repression of TNF-α or NO induced by KL-1037. These data suggest that microglial inactivation by KL-1037 is at least in part due to activation of PKA pathway and/or upregulation of IL-10. Thus, repressing proinflammatory cytokines and iNOS gene expression in activated microglia by KL-1037 may provide potential therapeutic strategies for various neurodegenerative diseases including ischemic cerebral disease. © 2004 Elsevier Ltd. All rights reserved.*
dc.languageEnglish*
dc.titleA new anti-inflammatory agent KL-1037 represses proinflammatory cytokine and inducible nitric oxide synthase (iNOS) gene expression in activated microglia*
dc.typeArticle*
dc.relation.issue2*
dc.relation.volume47*
dc.relation.indexSCI*
dc.relation.indexSCIE*
dc.relation.indexSCOPUS*
dc.relation.startpage243*
dc.relation.lastpage252*
dc.relation.journaltitleNeuropharmacology*
dc.identifier.doi10.1016/j.neuropharm.2004.03.019*
dc.identifier.wosidWOS:000222841100010*
dc.identifier.scopusid2-s2.0-3042513502*
dc.author.googleKim W.-K.*
dc.author.googleJang P.-G.*
dc.author.googleWoo M.-S.*
dc.author.googleHan I.-O.*
dc.author.googlePiao H.Z.*
dc.author.googleLee K.*
dc.author.googleLee H.*
dc.author.googleJoh T.H.*
dc.author.googleKim H.-S.*
dc.contributor.scopusid김원기(34770946200)*
dc.contributor.scopusid김희선(57191372551)*
dc.date.modifydate20240118140922*
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자연과학대학 > 화학·나노과학전공 > Journal papers
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