Full metadata record
DC Field | Value | Language |
---|---|---|
dc.contributor.author | 김원기 | * |
dc.contributor.author | 김희선 | * |
dc.date.accessioned | 2016-08-28T11:08:25Z | - |
dc.date.available | 2016-08-28T11:08:25Z | - |
dc.date.issued | 2004 | * |
dc.identifier.issn | 0028-3908 | * |
dc.identifier.other | OAK-12806 | * |
dc.identifier.uri | https://dspace.ewha.ac.kr/handle/2015.oak/228877 | - |
dc.description.abstract | Excessive 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.language | English | * |
dc.title | A new anti-inflammatory agent KL-1037 represses proinflammatory cytokine and inducible nitric oxide synthase (iNOS) gene expression in activated microglia | * |
dc.type | Article | * |
dc.relation.issue | 2 | * |
dc.relation.volume | 47 | * |
dc.relation.index | SCI | * |
dc.relation.index | SCIE | * |
dc.relation.index | SCOPUS | * |
dc.relation.startpage | 243 | * |
dc.relation.lastpage | 252 | * |
dc.relation.journaltitle | Neuropharmacology | * |
dc.identifier.doi | 10.1016/j.neuropharm.2004.03.019 | * |
dc.identifier.wosid | WOS:000222841100010 | * |
dc.identifier.scopusid | 2-s2.0-3042513502 | * |
dc.author.google | Kim W.-K. | * |
dc.author.google | Jang P.-G. | * |
dc.author.google | Woo M.-S. | * |
dc.author.google | Han I.-O. | * |
dc.author.google | Piao H.Z. | * |
dc.author.google | Lee K. | * |
dc.author.google | Lee H. | * |
dc.author.google | Joh T.H. | * |
dc.author.google | Kim H.-S. | * |
dc.contributor.scopusid | 김원기(34770946200) | * |
dc.contributor.scopusid | 김희선(57191372551) | * |
dc.date.modifydate | 20240118140922 | * |