(−)-Epigallocatechin-3-gallate inhibits monocyte chemotactic protein-1 expression in endothelial cells via blocking NF-κB signaling
| Autor: | Bong Whan Ahn, Mi H. Kim, Young Do Jung, Boo A. Shin, Nam H. Kim, Hee J. Chang, Min H. Hong |
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| Rok vydání: | 2007 |
| Předmět: |
MAPK/ERK pathway
p38 mitogen-activated protein kinases Blotting Western Electrophoretic Mobility Shift Assay Enzyme-Linked Immunosorbent Assay CCL2 p38 Mitogen-Activated Protein Kinases Catechin Monocytes General Biochemistry Genetics and Molecular Biology chemistry.chemical_compound Cell Movement medicine Humans General Pharmacology Toxicology and Pharmaceutics Promoter Regions Genetic Protein kinase A Chemokine CCL2 Chemistry Kinase Monocyte NF-kappa B Endothelial Cells General Medicine Blotting Northern Culture Media Cell biology medicine.anatomical_structure Gene Expression Regulation Phorbol Tetradecanoylphorbol Acetate Signal transduction Signal Transduction |
| Zdroj: | Life Sciences. 80:1957-1965 |
| ISSN: | 0024-3205 |
| DOI: | 10.1016/j.lfs.2007.02.024 |
| Popis: | 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. |
| Databáze: | OpenAIRE |
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