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首页> 外文期刊>Life sciences >-)-Epigallocatechin-3-gallate inhibits monocyte chemotactic protein-1 expression in endothelial cells via blocking NF-kappaB signaling.
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-)-Epigallocatechin-3-gallate inhibits monocyte chemotactic protein-1 expression in endothelial cells via blocking NF-kappaB signaling.

机译：-）-Epigallocatechin-3-gallate通过阻断NF-κB信号传导抑制内皮细胞中单核细胞趋化蛋白1的表达。

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摘要

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.
机译：单核细胞趋化蛋白-1（MCP-1）是单核细胞的有效化学引诱剂，在包括动脉粥样硬化在内的各种炎症反应中起关键作用。在这项研究中，我们检查了主要绿茶儿茶素（-）-epigallocatechin-3-gallate（EGCG）对人内皮ECV304细胞中MCP-1表达的影响。 EGCG以剂量依赖性方式显着抑制佛波醇12-肉豆蔻酸酯13-乙酸酯（PMA）诱导的MCP-1 mRNA和蛋白水平。还发现EGCG降低了MCP-1的转录活性。 PMA对MCP-1的上调被P38丝裂原活化蛋白激酶（MAPK）和NF-κB的阻断所显着抑制，但没有被细胞外信号调节的激酶和c-Jun N端激酶途径所阻断。此外，用EGCG预处理ECV304细胞后，PMA诱导的p38 MAPK和NF-κB活化明显减弱。来自经PMA处理的内皮ECV304细胞的条件培养基可显着刺激THP-1单核细胞的迁移，而MCP-1中和抗体可部分废除这种作用。此外，来自EGCG预处理的ECV304细胞的培养基失去了THP-1迁移的刺激活性。这些结果表明，EGCG可通过至少部分地通过抑制p38 MAPK和NF-κB激活介导的MCP-1表达来在内皮细胞中发挥抗炎作用。

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