Full metadata record
DC Field | Value | Language |
---|---|---|
dc.contributor.author | 김희선 | * |
dc.contributor.author | 박은미 | * |
dc.date.accessioned | 2016-08-28T12:08:04Z | - |
dc.date.available | 2016-08-28T12:08:04Z | - |
dc.date.issued | 2012 | * |
dc.identifier.issn | 0022-3565 | * |
dc.identifier.other | OAK-8566 | * |
dc.identifier.uri | https://dspace.ewha.ac.kr/handle/2015.oak/222451 | - |
dc.description.abstract | Microglial activation plays a pivotal role in the pathogenesis of various neurologic disorders, such as cerebral ischemia, Alzheimer's disease, and Parkinson's disease. Thus, controlling microglial activation is a promising therapeutic strategy for such brain diseases. In the present study, we found that a ginseng saponin metabolite, compound K [20-O-D-glucopyranosyl- 20(S)-protopanaxadiol], inhibited the expressions of inducible nitric-oxide synthase, proinflammatory cytokines, monocyte chemotactic protein-1, matrix metalloproteinase-3, and matrix metalloproteinase-9 in lipopolysaccharide (LPS)- stimulated BV2 microglial cells and primary cultured microglia. Subsequent mechanistic studies revealed that compound K suppressed microglial activation via inhibiting reactive oxygen species, mitogen-activated protein kinases, and nuclear factor-κB/ activator protein-1 activities with enhancement of heme oxygenase-1/antioxidant response element signaling. To address the anti-inflammatory effects of compound K in vivo, we used two brain disease models of mice: sepsis (systemic inflammation) and cerebral ischemia. Compound K reduced the number of Iba1-positive activated microglia and inhibited the expressions of tumor necrosis factor-α and interleukin-1β in the LPS-induced sepsis brain. Furthermore, compound K reduced the infarct volume of ischemic brain induced by middle cerebral artery occlusion and suppressed microglial activation in the ischemic cortex. The results collectively suggest that compound K is a promising agent for prevention and/or treatment of cerebral ischemia and other neuroinflammatory disorders. Copyright © 2012 by The American Society for Pharmacology and Experimental Therapeutics. | * |
dc.language | English | * |
dc.title | Anti-inflammatory mechanism of compound K in activated microglia and its neuroprotective effect on experimental stroke in mice | * |
dc.type | Article | * |
dc.relation.issue | 1 | * |
dc.relation.volume | 341 | * |
dc.relation.index | SCI | * |
dc.relation.index | SCIE | * |
dc.relation.index | SCOPUS | * |
dc.relation.startpage | 59 | * |
dc.relation.lastpage | 67 | * |
dc.relation.journaltitle | Journal of Pharmacology and Experimental Therapeutics | * |
dc.identifier.doi | 10.1124/jpet.111.189035 | * |
dc.identifier.wosid | WOS:000301530100007 | * |
dc.identifier.scopusid | 2-s2.0-84863388195 | * |
dc.author.google | Park J.-S. | * |
dc.author.google | Shin J.A. | * |
dc.author.google | Jung J.-S. | * |
dc.author.google | Hyun J.-W. | * |
dc.author.google | Van Le T.K. | * |
dc.author.google | Kim D.-H. | * |
dc.author.google | Park E.-M. | * |
dc.author.google | Kim H.-S. | * |
dc.contributor.scopusid | 김희선(57191372551) | * |
dc.contributor.scopusid | 박은미(35933416400) | * |
dc.date.modifydate | 20240123095000 | * |