title: Attenuation of monocyte adhesion and oxidised LDL uptake in luteolin-treated human endothelial cells exposed to oxidised LDL.
abstract: Oxidative modification of LDL is causally involved in the development of atherosclerosis and occurs in vivo in the blood as well as within the vascular wall. The present study attempted to explore whether polyphenolic flavonoids influence monocyte-endothelium interaction and lectin-like oxidised LDL receptor 1 (LOX-1) expression involved in the early development of atherosclerosis. The flavones luteolin and apigenin inhibited THP-1 cell adhesion onto oxidised LDL-activated human umbilical vein endothelial cells (HUVEC), while the flavanols of (-)epigallocatechin gallate and (+)catechin, the flavonols of quercetin and rutin, and the flavanones of naringin, naringenin, hesperidin and hesperetin did not have such effects. Consistently, Western blot analysis revealed that the flavones at 25 microM dramatically and significantly abolished HUVEC expression of vascular cell adhesion molecule-1 and E-selectin evidently enhanced by oxidised LDL; these inhibitory effects were exerted by drastically down regulating mRNA levels of these cell adhesion molecules. In addition, quercetin and luteolin significantly attenuated expression of LOX-1 protein up regulated in oxidised LDL-activated HUVEC with a fall in transcriptional mRNA levels of LOX-1. In addition, quercetin and luteolin clearly blunted oxidised LDL uptake by HUVEC treated with oxidised LDL. The results demonstrate that the flavones luteolin and apigenin as well as quercetin were effective in the different initial steps of atherosclerosis process by inhibiting oxidised LDL-induced endothelial monocyte adhesion and/or oxidised LDL uptake. Therefore, certain flavonoids qualify as anti-atherogenic agents in LDL systems, which may have implications for strategies attenuating endothelial dysfunction-related atherosclerosis.
authors.affiliation: Department of Food and Nutrition and Institute of Korea Nutrition Research, Hallym University, Chuncheon, South Korea.
authors.forename: Yu-Jin
authors.initials: YJ
authors.lastname: Jeong
authors.forename: Yean-Jung
authors.initials: YJ
authors.lastname: Choi
authors.forename: Jung-Suk
authors.initials: JS
authors.lastname: Choi
authors.forename: Hyang-Mi
authors.initials: HM
authors.lastname: Kwon
authors.forename: Sang-Wook
authors.initials: SW
authors.lastname: Kang
authors.forename: Ji-Young
authors.initials: JY
authors.lastname: Bae
authors.forename: Sang-Soo
authors.initials: SS
authors.lastname: Lee
authors.forename: Jung-Sook
authors.initials: JS
authors.lastname: Kang
authors.forename: Seoung Jun
authors.initials: SJ
authors.lastname: Han
authors.forename: Young-Hee
authors.initials: YH
authors.lastname: Kang
mesh_terms: D002448:Cell Adhesion / Q000187:drug effects; D015815:Cell Adhesion Molecules / Q000235:genetics / Q000378:metabolism; D002478:Cells, Cultured; D042783:Endothelial Cells / Q000166:cytology / Q000187:drug effects / Q000378:metabolism; D004730:Endothelium, Vascular / Q000166:cytology / Q000187:drug effects* / Q000378:metabolism; D006801:Humans; D008077:Lipoproteins, LDL / Q000493:pharmacokinetics / Q000494:pharmacology*; D047311:Luteolin / Q000494:pharmacology*; D009000:Monocytes / Q000166:cytology / Q000187:drug effects* / Q000378:metabolism; D011794:Quercetin / Q000494:pharmacology; D020133:Reverse Transcriptase Polymerase Chain Reaction / Q000379:methods; D051127:Scavenger Receptors, Class E / Q000037:antagonists & inhibitors; D015533:Transcriptional Activation / Q000187:drug effects
chemical_list: D015815:Cell Adhesion Molecules; D008077:Lipoproteins, LDL; C495137:OLR1 protein, human; D051127:Scavenger Receptors, Class E; C099252:oxidized low density lipoprotein; D011794:Quercetin; D047311:Luteolin