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

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

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

    min h hongMin H Hong,mi h kimMi H Kim,hee j changHee J Chang,nam h kimNam H Kim,boo a shinBoo A Shin,bong w ahnBong W Ahn,young d jungYoung D Jung,min h hongMin H Hong,mi h kimMi H Kim,hee j changHee J Chang,nam h kimNam H Kim,boo a shinBoo A Shin,bong w ahnBong W Ahn,young d jungYoung D Jung,

    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.

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

    mh hongMH Hong,mh kimMH Kim,hj changHJ Chang,nh kimNH Kim,ba shinBA Shin,bw ahnBW Ahn,yd jungYD Jung,mh hongMH Hong,mh kimMH Kim,hj changHJ Chang,nh kimNH Kim,ba shinBA Shin,bw ahnBW Ahn,yd jungYD Jung,

    For similar abstracts research abstracts see: abstracts research

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

    PUBLICATION TYPE: Research Support, Non-U.S. Gov

    Journal: Life sciences

    VOLUME: 80

    Page Numbers: 1957-65

    Journal Abbreviation:

    ISSN: 0024-3205

    DAY: 27

    MONTH: 02

    YEAR: 2007

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

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    LANGUAGE: eng

    NlmUniqueID: 375521

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    Grant and Affiliation Information for (-)-Epigallocatechin-3-gallate inhibits monocyte chemotactic protein-1 expression in endothelial cells via blocking NF-kappaB signaling.

    AFFILIATION: Chonnam University Research Institute of Medical Sciences, Chonnam National University Medical School, Kwangju, 501-190, South Korea.

    Country: England

    England Research PublicationEngland Research Publication

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    MEDLINETA: Life Sci

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