The green tea polyphenol (-)-epigallocatechin-3-gallate inhibits leukocyte activation by bacterial formylpeptide through the receptor FPR.
The green tea polyphenol (-)-epigallocatechin-3-gallate inhibits leukocyte activation by bacterial formylpeptide through the receptor FPR.
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DOI：
10.1016/j.intimp.2009.05.002
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发表时间：
2009-08
影响因子：
5.6
通讯作者：
Le Y
中科院分区：
文献类型：
--
作者：
Zhu J;Wang O;Ruan L;Hou X;Cui Y;Wang JM;Le Y
虽然绿茶多酚儿茶素被认为是一种潜在的抗炎剂，但其对细菌成分引起的炎症的影响却很少被研究。我们研究了没食子儿茶素没食子酸酯（EGCG）调节白细胞对细菌趋化肽n-甲酰基蛋氨酸-leucyl-苯丙氨酸（fMLF）的反应的能力，fMLF被吞噬白细胞上的人G蛋白偶联受体FPR识别。用EGCG预处理人单核细胞或转染fpr的大鼠嗜碱性白血病细胞（ETFR细胞）可显著抑制fmlf诱导的趋化性。小鼠腹腔注射EGCG可抑制fmlf诱导的白细胞向皮肤中形成的气囊浸润。机制研究表明，EGCG剂量依赖性地抑制fmlf诱导的单核细胞和ETFR细胞的钙通量。fmlf诱导的ETFR细胞迁移被一种特异性MEK1/2抑制剂PD98059显著抑制，这与fmlf诱导的ERK1/2磷酸化减少有关。这些结果表明EGCG抑制fpr介导的白细胞活化，因此是一种有前途的抗炎化合物。
Although green tea polyphenol catechin is considered as a potential anti-inflammatory agent, its effect on bacterial component-induced inflammation has been poorly investigated. We examined the capacity of epigallocatechin gallate (EGCG) to regulate leukocyte responses to bacterial chemotactic peptide N-formylmethionyl-leucyl-phenylalanine (fMLF), which is recognized by a human G protein-coupled receptor FPR on phagocytic leukocytes. Pretreatment of human monocytic cells or FPR-transfected rat basophilic leukemia cells (ETFR cells) with EGCG significantly inhibited fMLF-induced chemotaxis. Intraperitoneal administration of EGCG in mice suppressed fMLF-induced leukocyte infiltration into the air pouch created in the skin. Mechanistic studies revealed that EGCG dose-dependently suppressed fMLF-induced calcium flux in monocytic cells and ETFR cells. fMLF-induced ETFR cell migration was significantly inhibited by a specific MEK1/2 inhibitor, PD98059, which was associated with reduction in fMLF-induced ERK1/2 phosphorylation. These results suggest that EGCG inhibits FPR-mediated leukocyte activation thus is a promising anti-inflammatory compound.
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影响因子：
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