Bisacurone inhibits adhesion of inflammatory monocytes or cancer cells to endothelial cells through down-regulation of VCAM-1 expression

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dc.contributor.authorD I Sun-
dc.contributor.authorI T Nizamutdinova-
dc.contributor.authorY M Kim-
dc.contributor.authorX F Cai-
dc.contributor.authorJung Joon Lee-
dc.contributor.authorS S Kang-
dc.contributor.authorY S Kim-
dc.contributor.authorK M Kang-
dc.contributor.authorG Y Chai-
dc.contributor.authorK C Chang-
dc.contributor.authorH J Kim-
dc.date.accessioned2017-04-19T09:11:13Z-
dc.date.available2017-04-19T09:11:13Z-
dc.date.issued2008-
dc.identifier.issn1567-5769-
dc.identifier.uri10.1016/j.intimp.2008.05.006ko
dc.identifier.urihttps://oak.kribb.re.kr/handle/201005/8519-
dc.description.abstractBisacurone, one of the active compounds of the traditionally used indigenous herb Curcuma longa Linne (Zingiberaceae), has anti-oxidant, anti-inflammatory, and anti-metastatic activities. We studied how the level of vascular cell adhesion molecule-1 (VCAM-1), one of the key molecules in the development of atherosclerosis as well as carcinogenesis and metastasis, might be affected by bisacurone in tumor necrosis factor-alpha (TNF-α)-activated human umbilical vein endothelial cells (HUVECs). Bisacurone dose-dependently inhibited TNF-α-mediated expression of VCAM-1. It showed significant suppressive effect on ROS generation in response to TNF-α stimulation and it blocked nuclear factor-kappa B (NF-κB) p65 translocation into the nucleus and phosphorylation of inhibitory factor κBα (IκBα). It also inhibited phosphorylation of Akt and PKC, which are upstream in the regulation of VCAM-1 by TNF-α. Furthermore, bisacurone decreased U937 monocyte and human oral cancer cell (Hep-2, QLL-I, SCC-15) adhesion to HUVECs stimulated by TNF-α, suggesting that it may inhibit the binding of these cells by regulating the expression of critical adhesion molecules by TNF-α. Thus, bisacurone may be beneficial in the treatment of inflammatory diseases, such as atherosclerosis, where inflammatory monocytes are involved in their pathology, and, moreover, in the development of tumors.-
dc.publisherElsevier-
dc.titleBisacurone inhibits adhesion of inflammatory monocytes or cancer cells to endothelial cells through down-regulation of VCAM-1 expression-
dc.title.alternativeBisacurone inhibits adhesion of inflammatory monocytes or cancer cells to endothelial cells through down-regulation of VCAM-1 expression-
dc.typeArticle-
dc.citation.titleInternational Immunopharmacology-
dc.citation.number9-
dc.citation.endPage1281-
dc.citation.startPage1272-
dc.citation.volume8-
dc.contributor.affiliatedAuthorJung Joon Lee-
dc.contributor.alternativeName선동일-
dc.contributor.alternativeNameNizamutdinova-
dc.contributor.alternativeName김영민-
dc.contributor.alternativeNameCai-
dc.contributor.alternativeName이정준-
dc.contributor.alternativeName강삼식-
dc.contributor.alternativeName김영식-
dc.contributor.alternativeName강기문-
dc.contributor.alternativeName채규영-
dc.contributor.alternativeName장기철-
dc.contributor.alternativeName김혜정-
dc.identifier.bibliographicCitationInternational Immunopharmacology, vol. 8, no. 9, pp. 1272-1281-
dc.identifier.doi10.1016/j.intimp.2008.05.006-
dc.subject.keywordBisacurone-
dc.subject.keywordInflammatory disease-
dc.subject.keywordMetastasis-
dc.subject.keywordNF-kappa B-
dc.subject.keywordReactive oxygen species-
dc.subject.keywordVascular cell adhesion molecule-1-
dc.subject.localBisacurone-
dc.subject.localinflammatory disease-
dc.subject.localInflammatory disease-
dc.subject.localmetastasis-
dc.subject.localMetastasis-
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.subject.localReactive oxidative species-
dc.subject.localReactive oxygen species(ROS)-
dc.subject.localReactive oxygen species-
dc.subject.localReactive Oxygen Species (ROS)-
dc.subject.localReactive Oxygen Species-
dc.subject.localROS-
dc.subject.localReactive oxygen species (ROS)-
dc.subject.localreactive oxygen species-
dc.subject.localreactive oxygen species (ROS)-
dc.subject.localVascular cell adhesion molecule-1 (VCAM-1)-
dc.subject.localVascular cell adhesion molecule-1-
dc.subject.localvascular cell adhesion molecule-1-
dc.description.journalClassY-
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