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- Title
Epigallocatechin-3-O-gallate Decreases Tumor Necrosis Factor-α–induced Fractalkine Expression in Endothelial Cells by Suppressing NF-κB.
- Authors
Ae Sin Lee; Yu Jin Jung; Duk Hoon Kim; Tae Hwan Lee; Kyung Pyo Kang; Sik Lee; Nae Ho Lee; Mi Jeong Sung; Dae Young Kwon; Sung Kwang Park; Won Kim
- Abstract
Epigallocatechin-3-O-gallate (EGCG), the main catechin in green tea, has anti-oxidant, anti-atherosclerotic and anti-inflammatory properties. Fractalkine, a chemokine involved in inflammation and early atherosclerotic processes, acts as a chemoattractant as well as an adhesion molecule in endothelial cells activated by proinflammatory cytokines. In the present study, we investigated the effect of EGCG on fractalkine expression in TNF-α-induced human umbilical vein endothelial cells (HUVECs). EGCG decreased TNF-α-induced fractalkine mRNA and protein expression in HUVECs in a time-dependent manner. EGCG suppressed the TNF-α-induced phosphorylation and degradation of IκB-α, thereby decreasing the phosphorylation and nuclear translocation of the NF-κB p65 subunit in HUVECs. The DNA binding activity of the NF-κB p65 subunit was lower in EGCG-pretreated HUVECs than in those treated with TNF-α alone. Furthermore, EGCG inhibited monocyte adhesion to HUVECs stimulated by TNF-α. The silencing of fractalkine with an siRNA or treatment with a blocking antibody against fractalkine suppressed the TNF-α-induced increase in monocyte adhesion. These results demonstrate that EGCG prevents TNF-α-induced vascular endothelial fractalkine expression. Copyright © 2009 S. Karger AG, Basel
- Subjects
EPIGALLOCATECHIN gallate; TUMOR necrosis factors; ENDOTHELIUM; CELLULAR immunity; CYTOKINES; TUMORS; ATHEROSCLEROSIS
- Publication
Cellular Physiology & Biochemistry (Karger AG), 2009, Vol 24, Issue 5/6, p503
- ISSN
1015-8987
- Publication type
Article
- DOI
10.1159/000257494