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Ginsenoside metabolite compound K differentially antagonizing tumor necrosis factor-α-induced monocyte-endothelial trafficking : Ginsenoside metabolite compound K differentially antagonizing tumor necrosis factor-alpha-induced monocyte-endothelial trafficking

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dc.contributor.authorLee, Eun-Sook-
dc.contributor.authorChoi, Jung-Suk-
dc.contributor.authorKim, Min Soo-
dc.contributor.authorYou, Hyun Ju-
dc.contributor.authorJi, Geun Eog-
dc.contributor.authorKang, Young-Hee-
dc.date.accessioned2024-05-01T01:36:45Z-
dc.date.available2024-05-01T01:36:45Z-
dc.date.created2021-10-21-
dc.date.issued2011-10-
dc.identifier.citationChemico-Biological Interactions, Vol.194 No.1, pp.13-22-
dc.identifier.issn0009-2797-
dc.identifier.urihttps://hdl.handle.net/10371/200205-
dc.description.abstractHuman leukocyte endothelial adhesion and transmigration occur in the early stage of the pathogenesis of atherosclerosis. Vascular endothelial cells are targeted by pro-inflammatory cytokines modulating many gene proteins responsible for cell adhesion, thrombosis and inflammatory responses. This study examined the potential of compound K to inhibit the pro-inflammatory cytokine TNF-alpha, induction of monocyte adhesion onto TNF-alpha-activated human umbilical vein endothelial cells (HUVEC). HUVEC were cultured with 10 ng/ml TNF-alpha with individual ginsenosides of Rb1, Rc, Re, Rhl and compound K (CK). Ginsenosides at doses of <= 50 mu M did not show any cytotoxicity. TNF-alpha induced THP-1 monocyte adhesion to HUVEC, and such induction was attenuated by Rh1 and CK. Consistently, CK suppressed TNF-alpha-induced expression of HUVEC adhesion molecules of VCAM-1, ICAM-1 and E-selectin, and also Rhl showed a substantial inhibition. Rh1 and CK dampened induction of counter-receptors, alpha 4/beta 1 integrin VLA-4 and alpha L/beta 2 integrin LFA-1 in TNF-alpha-treated THP-1 cells. Additionally, CK diminished THP-1 secretion of MMP-9 required during transmigration, inhibiting transendothelial migration of THP-1 cells. CK blunted TNF-alpha-promoted IL-8 secretion of HUVEC and CXCR1 expression of THP-1 monocytes. Furthermore, INF-alpha-activated endothelial I kappa B phosphorylation and NF-kappa B nuclear translocation were disturbed by CK, and TNF-alpha induction of alpha 4/beta 1 integrin was abrogated by the NF-kappa B inhibitor SN50. These results demonstrate that CK exerts anti-atherogenic activity with blocking leukocyte endothelial interaction and transmigration through negatively mediating NF-kappa B signaling. (C) 2011 Elsevier Ireland Ltd. All rights reserved.-
dc.language영어-
dc.publisherElsevier BV-
dc.titleGinsenoside metabolite compound K differentially antagonizing tumor necrosis factor-α-induced monocyte-endothelial trafficking-
dc.title.alternativeGinsenoside metabolite compound K differentially antagonizing tumor necrosis factor-alpha-induced monocyte-endothelial trafficking-
dc.typeArticle-
dc.identifier.doi10.1016/j.cbi.2011.08.008-
dc.citation.journaltitleChemico-Biological Interactions-
dc.identifier.wosid000296994800002-
dc.identifier.scopusid2-s2.0-80052835896-
dc.citation.endpage22-
dc.citation.number1-
dc.citation.startpage13-
dc.citation.volume194-
dc.description.isOpenAccessN-
dc.contributor.affiliatedAuthorYou, Hyun Ju-
dc.contributor.affiliatedAuthorJi, Geun Eog-
dc.type.docTypeArticle-
dc.description.journalClass1-
dc.subject.keywordPlusFACTOR-KAPPA-B-
dc.subject.keywordPlusIN-VITRO-
dc.subject.keywordPlusTRANSENDOTHELIAL MIGRATION-
dc.subject.keywordPlusCELL-ADHESION-
dc.subject.keywordPlusUP-REGULATION-
dc.subject.keywordPlusEXPRESSION-
dc.subject.keywordPlusPATHWAYS-
dc.subject.keywordPlusRH1-
dc.subject.keywordPlusATHEROSCLEROSIS-
dc.subject.keywordPlusTRANSMIGRATION-
dc.subject.keywordAuthorAdhesion molecules-
dc.subject.keywordAuthorCompound K-
dc.subject.keywordAuthorGinsenoside-
dc.subject.keywordAuthorIntegrin-
dc.subject.keywordAuthorTransendothelial migration-
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  • College of Human Ecology
  • Department of Food and Nutrition
Research Area Biochemistry & Molecular Biology, Food Science & Technology, Microbiology, 미생물학, 분자생물학, 식품공학

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