Full metadata record
DC Field | Value | Language |
---|---|---|
dc.contributor.author | 오구택 | * |
dc.date.accessioned | 2018-05-18T08:15:10Z | - |
dc.date.available | 2018-05-18T08:15:10Z | - |
dc.date.issued | 2005 | * |
dc.identifier.issn | 0022-3565 | * |
dc.identifier.other | OAK-2673 | * |
dc.identifier.uri | https://dspace.ewha.ac.kr/handle/2015.oak/243165 | - |
dc.description.abstract | This study shows that 6-[4-(1-cyclohexyl-1H-tetrazol-5-yl) butoxy]-3,4-dihydro-2(1H)-quinolinone (cilostazol) suppresses the atherosclerotic lesion formation in the low-density lipoprotein receptor (Ldlr)-null mice. Ldlr-null mice fed a high cholesterol diet showed multiple plaque lesions in the proximal ascending aorta including aortic sinus, accompanied by increased macrophage accumulation with increased expression of vascular cell adhesion molecule-1 (VCAM-1) and monocyte chemoattractant protein-1 (MCP-1). Supplementation of cilostazol (0.2% w/w) in diet significantly decreased the plaque lesions with reduced macrophage accumulation and suppression of VCAM-1 and MCP-1 in situ. Increased superoxide and tumor necrosis factor-α (TNF-α) production were significantly lowered by cilostazol in situ as well as in cultured human umbilical vein endothelial cells (HUVECs). TNF-α-induced increased inhibitory κBα degradation in the cytoplasm and nuclear factor-κB (NF-κB) p65 activation in the nuclei of HUVECs were reversed by cilostazol (1 ∼ 100 μM) as well as by (E)-3[(4-t-butylphenyl)sulfonyl]-2-propenenitrile (BAY 11-7085) (10 μM), suggesting that cilostazol strongly inhibits NF-κB activation and p65 translocation into the nuclei. Furthermore, in gel shift and DNA-binding assay, cilostazol inhibited NF-κB/DNA complex and nuclear DNA-binding activity of the NF-κB in the nuclear extracts of the RAW 264.7 cells. Taken together, it is suggested that the antiatherogenic effect of cilostazol in cholesterol-fed Ldlr-null mice is ascribed to its property to suppress superoxide and TNF-α formation, and thereby reducing NF-κB activation/transcription, VCAM-1/MCP-1 expressions, and monocyte recruitments. Copyright © 2005 by The American Society for Pharmacology and Experimental Therapeutics. | * |
dc.language | English | * |
dc.title | Cilostazol reduces atherosclerosis by inhibition of superoxide and tumor necrosis factor-α formation in low-density lipoprotein receptor-null mice fed high cholesterol | * |
dc.type | Article | * |
dc.relation.issue | 2 | * |
dc.relation.volume | 313 | * |
dc.relation.index | SCI | * |
dc.relation.index | SCIE | * |
dc.relation.index | SCOPUS | * |
dc.relation.startpage | 502 | * |
dc.relation.lastpage | 509 | * |
dc.relation.journaltitle | Journal of Pharmacology and Experimental Therapeutics | * |
dc.identifier.doi | 10.1124/jpet.104.079780 | * |
dc.identifier.wosid | WOS:000228357900003 | * |
dc.identifier.scopusid | 2-s2.0-20944448650 | * |
dc.author.google | Lee J.H. | * |
dc.author.google | Oh G.T. | * |
dc.author.google | Park S.Y. | * |
dc.author.google | Choi J.-H. | * |
dc.author.google | Park J.-G. | * |
dc.author.google | Kim C.D. | * |
dc.author.google | Lee W.S. | * |
dc.author.google | Rhim B.Y. | * |
dc.author.google | Shin Y.W. | * |
dc.author.google | Hong K.W. | * |
dc.contributor.scopusid | 오구택(7007056663) | * |
dc.date.modifydate | 20240123094756 | * |