• Antje Ludwig, Mario Lorenz, Nicole Grimbo, Frederike Steinle, Silke Meiners, Cornelia Bartsch, Karl Stangl, Gert Baumann, and Verena Stangl.
• Medizinische Klinik und Poliklinik, Schwerpunkt Kardiologie, Angiologie, Pneumologie Charité der Humboldt-Universität, Campus Mitte, Berlin, Germany.
• Biochem. Biophys. Res. Commun. 2004 Apr 9; 316 (3): 659-65.

AbstractAttachment 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.

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