(-)-Epigallocatechin-3-gallate inhibits monocyte chemotactic protein-1 expression in endothelial cells via blocking NF-kappaB signaling

Monocyte chemotactic protein-1 (MCP-1) is a potent chemoattractant for monocytes and plays a key role in various inflammatory responses, including atherosclerosis. In this study, we examined the effect of (-)-epigallocatechin-3-gallate (EGCG), a major green tea catechin, on the expression of MCP-1 i...

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Bibliographic Details
Published in:Life sciences (1973) 2007-05, Vol.80 (21), p.1957
Main Authors: Hong, Min H, Kim, Mi H, Chang, Hee J, Kim, Nam H, Shin, Boo A, Ahn, Bong W, Jung, Young D
Format: Article
Language:English
Subjects:
Blotting, Northern
Blotting, Western
Catechin - analogs & derivatives
Catechin - pharmacology
Cell Movement - drug effects
Chemokine CCL2 - genetics
Chemokine CCL2 - metabolism
Culture Media - pharmacology
Electrophoretic Mobility Shift Assay
Endothelial Cells - drug effects
Endothelial Cells - metabolism
Enzyme-Linked Immunosorbent Assay
Gene Expression Regulation - drug effects
Humans
Monocytes - drug effects
NF-kappa B - metabolism
p38 Mitogen-Activated Protein Kinases - metabolism
Promoter Regions, Genetic - genetics
Signal Transduction - drug effects
Tetradecanoylphorbol Acetate - metabolism
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Summary:Monocyte chemotactic protein-1 (MCP-1) is a potent chemoattractant for monocytes and plays a key role in various inflammatory responses, including atherosclerosis. In this study, we examined the effect of (-)-epigallocatechin-3-gallate (EGCG), a major green tea catechin, on the expression of MCP-1 in human endothelial ECV304 cells. EGCG markedly inhibited the phorbol 12-myristate 13-acetate (PMA)-induced MCP-1 mRNA and protein levels in a dose-dependent manner. EGCG was also found to reduce the MCP-1 transcriptional activity. The upregulation of MCP-1 by PMA was significantly inhibited by blockade of P38 mitogen-activated protein kinase (MAPK) and NF-kappaB, but not by blockade of extracellular-signal-regulated kinase and c-Jun N-terminal kinase pathway. Furthermore, The PMA-induced p38 MAPK and NF-kappaB activation were obviously attenuated after pretreating ECV304 cells with EGCG. The conditioned media from the endothelial ECV304 cells treated with PMA could remarkably stimulate the migration of THP-1 monocytes and this effect was partially abrogated by MCP-1 neutralizing antibodies. Moreover, the media from the EGCG-pretreated ECV304 cells lost the stimulatory activity for THP-1 migration. These results suggest that EGCG may exert an anti-inflammatory effect in endothelial cells by controlling MCP-1 expression, at least in part, mediated through the suppression of p38 MAPK and NF-kappaB activation.
ISSN:0024-3205