Full metadata record
DC Field | Value | Language |
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dc.contributor.author | Jeong, Jin-Woo | - |
dc.contributor.author | Lee, Hye Hyeon | - |
dc.contributor.author | Han, Min Ho | - |
dc.contributor.author | Kim, Gi-Young | - |
dc.contributor.author | Kim, Wun-Jae | - |
dc.contributor.author | Choi, Yung Hyun | - |
dc.date.available | 2017-07-11T05:26:34Z | - |
dc.date.created | 2017-04-10 | - |
dc.date.issued | 2014-04 | - |
dc.identifier.issn | 0009-2797 | - |
dc.identifier.uri | http://hdl.handle.net/20.500.11750/2657 | - |
dc.description.abstract | Genistein, a principal soy isoflavone, has received considerable attention as a protein kinase inhibitor. Although some studies have demonstrated that genistein possesses anti-inflammatory effects, the molecular mechanisms of genistein-mediated anti-inflammatory potential are unclear in microglial cells. In this study, we determined whether genistein attenuates pro-inflammatory responses in lipopolysaccharide (LPS)-stimulated BV2 microglia and attempted to establish the possible mechanisms. Our results indicated that genistein inhibited the production of nitric oxide (NO) and prostaglandin E2 at non-toxic concentrations by inhibiting inducible NO synthase and cyclooxygenase-2 expression. The increased release and expression of inflammatory cytokines, including interleukin-1β, tumor necrosis factor-α, by LPS, were markedly reduced by genistein. Genistein also attenuated LPS-induced reactive oxygen species generation and LPS-mediated nuclear translocation of nuclear factor-kappa B (NF-κB), associated with blocking degradation of the inhibitor of NF-κB-α. Furthermore, genistein potently suppressed binding of LPS to the microglial cell surface, indicating the antagonistic effect of genistein against toll like receptor 4 (TLR4), and inhibited LPS-induced TLR4 and myeloid differentiation factor 88 expression. In addition, blocking TLR4 signaling using the specific TLR4 signaling inhibitor CLI-095 increased the anti-inflammatory potential of genistein in BV2 microglia. Our data indicate that genistein may attenuate the initiation of intracellular signaling cascades by LPS through inhibiting NF-κB activation by inhibiting the binding of LPS to TLR-4 on microglial cells. ©2014 Elsevier Ireland Ltd. All rights reserved. | - |
dc.language | English | - |
dc.publisher | Elsevier | - |
dc.title | Anti-inflammatory effects of genistein via suppression of the toll-like receptor 4-mediated signaling pathway in lipopolysaccharide-stimulated BV2 microglia | - |
dc.type | Article | - |
dc.identifier.doi | 10.1016/j.cbi.2014.01.012 | - |
dc.identifier.scopusid | 2-s2.0-84894091562 | - |
dc.identifier.bibliographicCitation | Chemico: Biological Interactions, v.212, pp.30 - 39 | - |
dc.description.isOpenAccess | FALSE | - |
dc.subject.keywordAuthor | Genistein | - |
dc.subject.keywordAuthor | BV2 microglia | - |
dc.subject.keywordAuthor | Anti-inflammation | - |
dc.subject.keywordAuthor | NF-kappa B | - |
dc.subject.keywordAuthor | TLR4 | - |
dc.subject.keywordPlus | NITRIC-OXIDE SYNTHASE | - |
dc.subject.keywordPlus | KAPPA-B ACTIVATION | - |
dc.subject.keywordPlus | INFLAMMATORY RESPONSE | - |
dc.subject.keywordPlus | OXIDATIVE STRESS | - |
dc.subject.keywordPlus | SYSTEMIC INFLAMMATION | - |
dc.subject.keywordPlus | NEURODEGENERATION | - |
dc.subject.keywordPlus | PROTEIN | - |
dc.subject.keywordPlus | POLYPHENOLS | - |
dc.subject.keywordPlus | DISEASES | - |
dc.subject.keywordPlus | CELLS | - |
dc.citation.endPage | 39 | - |
dc.citation.startPage | 30 | - |
dc.citation.title | Chemico: Biological Interactions | - |
dc.citation.volume | 212 | - |
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