Full metadata record
DC Field | Value | Language |
---|---|---|
dc.contributor.author | 김희선 | * |
dc.contributor.author | 박진선 | * |
dc.date.accessioned | 2016-08-28T12:08:06Z | - |
dc.date.available | 2016-08-28T12:08:06Z | - |
dc.date.issued | 2008 | * |
dc.identifier.issn | 1567-5769 | * |
dc.identifier.other | OAK-5196 | * |
dc.identifier.uri | https://dspace.ewha.ac.kr/handle/2015.oak/220091 | - |
dc.description.abstract | Previously, we and others have demonstrated that wogonin, an active component from the root of Scutellaria baicalensis Georgi, has a neuroprotective effect in cerebral ischemic insult. The neuroprotective effect of wogonin may at least in part be due to its anti-inflammatory properties. Microglial cells, well-known residential macrophages in the central nervous system, migrate to the ischemic lesion and play a pivotal role in the development of chronic inflammation. In the present study, we observed that wogonin potently inhibited microglial migration toward a chemokine, monocyte chemoattractant protein-1 (MCP-1). The anti-migratory effect of wogonin was provoked at nanomolar concentrations, at which wogonin did not significantly inhibit the production of cytokines and chemokines. NF-κB has previously shown to regulate microglial cell migration, and activation of cAMP-signaling pathway has also been associated with inhibition of microglial cell motility. In the present study, wogonin at low micromolar concentrations completely suppressed the activity of NF-κB in MCP-1-stimulated microglia, and NF-κB inhibitors such as N-acetyl cysteine and pyrrolidinedithiocarbamate inhibited the MCP-1-induced migration of microglial cells. However, wogonin did not stimulate the production of cAMP in microglial cells. Our results indicate that the anti-inflammatory activity of wogonin is exerted at least in part by suppressing microglial cell motility via inhibition of NF-κB activity. © 2008 Elsevier B.V. All rights reserved. | * |
dc.language | English | * |
dc.title | Wogonin inhibits microglial cell migration via suppression of nuclear factor-kappa B activity | * |
dc.type | Article | * |
dc.relation.issue | 12 | * |
dc.relation.volume | 8 | * |
dc.relation.index | SCI | * |
dc.relation.index | SCIE | * |
dc.relation.index | SCOPUS | * |
dc.relation.startpage | 1658 | * |
dc.relation.lastpage | 1662 | * |
dc.relation.journaltitle | International Immunopharmacology | * |
dc.identifier.doi | 10.1016/j.intimp.2008.07.018 | * |
dc.identifier.wosid | WOS:000260805100009 | * |
dc.identifier.scopusid | 2-s2.0-54549104761 | * |
dc.author.google | Piao H.Z. | * |
dc.author.google | Choi I.Y. | * |
dc.author.google | Park J.-S. | * |
dc.author.google | Kim H.-S. | * |
dc.author.google | Cheong J.H. | * |
dc.author.google | Son K.H. | * |
dc.author.google | Jeon S.J. | * |
dc.author.google | Ko K.H. | * |
dc.author.google | Kim W.-K. | * |
dc.contributor.scopusid | 김희선(57191372551) | * |
dc.contributor.scopusid | 박진선(54914743600) | * |
dc.date.modifydate | 20240215165648 | * |