KR-31378 ameliorates atherosclerosis by blocking monocyte recruitment in hypercholestrolemic mice

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dc.contributor.authorJi Yun Kim-
dc.contributor.authorKi Hoan nam-
dc.contributor.authorS O Kim-
dc.contributor.authorJae Hoon Choi-
dc.contributor.authorHyoung-Chin Kim-
dc.contributor.authorS D Yang-
dc.contributor.authorJoo Hyoung Kang-
dc.contributor.authorYoung Han Ryu-
dc.contributor.authorGoo Taeg Oh-
dc.contributor.authorS E Yoo-
dc.date.accessioned2017-04-19T09:00:59Z-
dc.date.available2017-04-19T09:00:59Z-
dc.date.issued2004-
dc.identifier.issn08926638-
dc.identifier.uri10.1055/s-2004-815545ko
dc.identifier.urihttps://oak.kribb.re.kr/handle/201005/6456-
dc.description.abstractThe recruitment of monocytes into the artery wall is a crucial early step in atherogenesis. A novel compound, KR-31378, has been shown to be a neuroprotective agent for ischemia-reperfusion damage in rat brain via its potent antioxidant and antiapoptotic actions. Here, we report the effects of this compound on atherogenesis and possible mechanisms of action. In Ldlr knockout mice fed with a high-fat, high-cholesterol diet, treatment with KR-31378 significantly inhibited fatty streak formation and macrophage accumulation. To address the possibility that KR-31378 may influence the initial stages of atherogenesis, we examined its effect on the adhesion and migration of monocytes to endothelial cells stimulated with tumor necrosis factor-alpha. KR-31378 decreased the adhesion in a dose-dependent manner. The observed decreases in cell adhesion and migration correlated with KR-31378-mediated down-regulation of vascular cell adhesion molecule-1 (VCAM-1) and interleukin (IL)-8. Nuclear factor-kappaB (NF-kappaB) is known to regulate the expression of adhesive and chemotactic molecules including VCAM-1 and IL-8. Indeed, transient transfection experiments, electrophoretic mobility shift assay, and IkappaB degradation assay showed that KR-31378 decreased NF-kappaB activation. These results indicate that KR-31378 potently reduces fatty streak formation by inhibiting NF-kappaB-dependent cellular adhesion and chemotactic molecule expression, which are crucial to monocyte infiltration into the arterial wall during the early stages of atherogenesis.-
dc.publisherWiley-
dc.titleKR-31378 ameliorates atherosclerosis by blocking monocyte recruitment in hypercholestrolemic mice-
dc.title.alternativeKR-31378 ameliorates atherosclerosis by blocking monocyte recruitment in hypercholestrolemic mice-
dc.typeArticle-
dc.citation.titleFASEB Journal-
dc.citation.number6-
dc.citation.endPage716-
dc.citation.startPage714-
dc.citation.volume18-
dc.contributor.affiliatedAuthorKi Hoan nam-
dc.contributor.affiliatedAuthorHyoung-Chin Kim-
dc.contributor.alternativeName김지윤-
dc.contributor.alternativeName남기환-
dc.contributor.alternativeName김선옥-
dc.contributor.alternativeName최재훈-
dc.contributor.alternativeName김형진-
dc.contributor.alternativeName양성돈-
dc.contributor.alternativeName강주형-
dc.contributor.alternativeName류영한-
dc.contributor.alternativeName오구택-
dc.contributor.alternativeName유성은-
dc.identifier.bibliographicCitationFASEB Journal, vol. 18, no. 6, pp. 714-716-
dc.identifier.doi10.1096/fj.03-0652fje-
dc.description.journalClassY-
Appears in Collections:
Ochang Branch Institute > Division of Bioinfrastructure > Laboratory Animal Resource Center > 1. Journal Articles
Ochang Branch Institute > Division of Bioinfrastructure > 1. Journal Articles
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