Isotrifoliol inhibits pro-inflammatory mediators by suppression of TLR/NF-κB and TLR/MAPK signaling in LPS-induced RAW264.7 cells

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dc.contributor.authorHua Li-
dc.contributor.authorJeong-Hyun Yoon-
dc.contributor.authorHyo Jun Won-
dc.contributor.authorHyeon-Seon Ji-
dc.contributor.authorHeong Joo Yuk-
dc.contributor.authorK H Park-
dc.contributor.authorHo Yong Park-
dc.contributor.authorTae Sook Jeong-
dc.date.accessioned2017-08-29-
dc.date.available2017-08-29-
dc.date.issued2017-
dc.identifier.issn1567-5769-
dc.identifier.uri10.1016/j.intimp.2017.01.033ko
dc.identifier.urihttps://oak.kribb.re.kr/handle/201005/17030-
dc.description.abstractSoybeans, produced by Glycine max (L.) Merr., contain high levels of isoflavones, such as genistein and daidzein. However, soy leaves contain more diverse and abundant flavonol glycosides and coumestans, as compared to the soybean. This study investigated the anti-inflammatory effects of the major coumestans present in soy leaf (coumestrol, isotrifoliol, and phaseol) in lipopolysaccharide (LPS)-induced RAW264.7 cells. Coumestans significantly reduced LPS-induced nitric oxide (NO), prostaglandin E2 (PGE2), and reactive oxygen species (ROS) production; isotrifoliol had the most potent anti-inflammatory activity. Isotrifoliol reduced LPS-mediated induction of mRNA expression of inducible nitric-oxide synthase (iNOS), cyclooxygenase-2 (COX-2), interleukin (IL)-1β, IL-6, tumor necrosis factor alpha (TNFα), and chemokines, such as chemokine (C-C motif) ligand (CCL) 2, CCL3, and CCL4. Isotrifoliol prevented NF-κB p65 subunit activation by reducing the phosphorylation and degradation of the inhibitor of NF-κB. And isotrifoliol significantly suppressed phosphorylation of the extracellular signal-regulated protein kinase 1/2 (ERK1/2) and p38 mitogen-activated protein kinase (MAPK). Furthermore, isotrifoliol suppressed LPS-induced Toll-like Receptor (TLR) signaling pathway, including mRNA expression of TNF receptor associated factor 6, transforming growth factor beta-activated kinase 1 (TAK1), TAK1 binding protein 2 (TAB2), and TAB3. These results demonstrate that isotrifoliol exerts an anti-inflammatory effect by suppressing the expression of inflammatory mediators via inhibition of TLR/NF-κB and TLR/MAPK signaling in LPS-induced RAW264.7 macrophages. Therefore, isotrifoliol can be used as an anti-inflammatory agent, and coumestan-rich soy leaf extracts may provide a useful dietary supplement.-
dc.publisherElsevier-
dc.titleIsotrifoliol inhibits pro-inflammatory mediators by suppression of TLR/NF-κB and TLR/MAPK signaling in LPS-induced RAW264.7 cells-
dc.title.alternativeIsotrifoliol inhibits pro-inflammatory mediators by suppression of TLR/NF-κB and TLR/MAPK signaling in LPS-induced RAW264.7 cells-
dc.typeArticle-
dc.citation.titleInternational Immunopharmacology-
dc.citation.number--
dc.citation.endPage119-
dc.citation.startPage110-
dc.citation.volume45-
dc.contributor.affiliatedAuthorHua Li-
dc.contributor.affiliatedAuthorJeong-Hyun Yoon-
dc.contributor.affiliatedAuthorHyo Jun Won-
dc.contributor.affiliatedAuthorHyeon-Seon Ji-
dc.contributor.affiliatedAuthorHeong Joo Yuk-
dc.contributor.affiliatedAuthorHo Yong Park-
dc.contributor.affiliatedAuthorTae Sook Jeong-
dc.contributor.alternativeName이화-
dc.contributor.alternativeName윤정현-
dc.contributor.alternativeName원효준-
dc.contributor.alternativeName지현선-
dc.contributor.alternativeName육흥주-
dc.contributor.alternativeName박기훈-
dc.contributor.alternativeName박호용-
dc.contributor.alternativeName정태숙-
dc.identifier.bibliographicCitationInternational Immunopharmacology, vol. 45, no. -, pp. 110-119-
dc.identifier.doi10.1016/j.intimp.2017.01.033-
dc.subject.keywordAnti-inflammation-
dc.subject.keywordCoumestans-
dc.subject.keywordIsotrifoliol-
dc.subject.keywordMacrophages-
dc.subject.keywordMAPK-
dc.subject.keywordNF-κB-
dc.subject.localantiinflammation-
dc.subject.localAntiinflammation-
dc.subject.localanti-inflammation-
dc.subject.localAnti-Inflammation-
dc.subject.localAnti-inflammation-
dc.subject.localCoumestan-
dc.subject.localCoumestans-
dc.subject.localIsotrifoliol-
dc.subject.localmacrophages-
dc.subject.localmacrophage-
dc.subject.localMacrophages-
dc.subject.localMacrophage-
dc.subject.localMAPK-
dc.subject.localMAPKs-
dc.subject.localNuclear factor-kappa B-
dc.subject.localnuclear factor κB-
dc.subject.localNf-κb-
dc.subject.localNF-kB-
dc.subject.localnuclear factor kappa B-
dc.subject.localNF-κB (nuclear factor kappa-B)-
dc.subject.localNF-kappaB-
dc.subject.localNuclear factor-κb-
dc.subject.localNF-κ B-
dc.subject.localNF-κB-
dc.subject.localNF-kappa B-
dc.subject.localNuclear factor κB (NF-κB)-
dc.subject.localNuclear factor κB-
dc.subject.localNFκB-
dc.subject.localNf-κB-
dc.subject.localNuclear factor-κB-
dc.subject.localnuclear factorκB-
dc.subject.localNuclear factor (NF)-κB-
dc.subject.localNuclear factor kappa B-
dc.subject.localnuclear factor-κB-
dc.subject.localNF-ΚB-
dc.subject.localNuclear factor-kappa B (NF-κB)-
dc.subject.localNuclear factor-kappaB-
dc.subject.localnuclear factor-kappaB-
dc.subject.localnuclear factor-kappaB (NF-κB)-
dc.subject.localNFkappaB-
dc.subject.localNuclear factor kappaB-
dc.description.journalClassY-
Appears in Collections:
Division of Biomedical Research > Microbiome Convergence Research Center > 1. Journal Articles
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