The tea flavonoid epigallocatechin-3-gallate reduces cytokine-induced VCAM-1 expression and monocyte adhesion to endothelial cells

被引:176
作者
Ludwig, A [1 ]
Lorenz, M [1 ]
Grimbo, N [1 ]
Steinle, F [1 ]
Meiners, S [1 ]
Bartsch, C [1 ]
Stangl, K [1 ]
Baumann, G [1 ]
Stangl, V [1 ]
机构
[1] Humboldt Univ, Charite, Med Klin & Poliklin, Berlin, Germany
关键词
atherosclerosis; tea catechins; cytokines; adhesion molecules;
D O I
10.1016/j.bbrc.2004.02.099
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Attachment of leukocytes to the vascular endothelium and the subsequent migration of cells into the vessel wall are early events in atherogenesis. This process requires the expression of endothelial adhesion molecules. Since tea catechins are reputed to promote antiatherogenic activities, we investigated the effects of various tea catechins-i.e., epicatechin (EC), epicatechin gallate (ECG), epigallocatechin (EGC), and epigallocatechin-3-gallate (EGCG)-on cytokine-induced expression of intercellular adhesion molecule-1 (ICAM-1), vascular cell adhesion molecule-1 (VCAM-1), and endothelial leukocyte adhesion molecule-1 (E-selectin) in HUVECs by ELISA. EGCG and to a lesser extent ECG prevented the induction of VCAM-1 expression in a concentration-dependent manner after stimulation with TNF-alpha, whereas EC and EGC were without effect. EGCG also inhibited the IL-1beta-induced induction of VCAM-1 expression. Inhibition of cytokine-induced VCAM-1 expression was manifested already on the transcriptional level. Furthermore, EGCG reduced the TNF-alpha-induced adhesion of THP-1 cells to HUVECs. EGCG did not influence TNF-alpha-stimulated NF-kappaB activation. (C) 2004 Elsevier Inc. All rights reserved.
引用
收藏
页码:659 / 665
页数:7
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