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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.accessioned 2023-07-25T14:40:18Z -
dc.date.available 2023-07-25T14:40:18Z -
dc.date.created 2017-04-10 -
dc.date.issued 2014-04 -
dc.identifier.issn 0009-2797 -
dc.identifier.uri http://hdl.handle.net/20.500.11750/46279 -
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.citation.endPage 39 -
dc.citation.startPage 30 -
dc.citation.title Chemico: Biological Interactions -
dc.citation.volume 212 -
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