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    請使用永久網址來引用或連結此文件: https://ir.lib.ncu.edu.tw/handle/987654321/102565


    題名: Green tea (–)-epigallocatechin gallate inhibits the growth of human villous trophoblasts via the ERK, p38, AMP-activated protein kinase, and protein kinase B pathways
    作者: 高永旭;Shih, Li-Jane;Chen, Tz-Fang;Lin, Cheng-Kuo;Liu, Hang-Shen;Kao, Yung-Hsi
    貢獻者: 生醫理工學院生命科學系
    關鍵詞: AMP-Activated Protein Kinases - metabolism;Androstadienes - pharmacology;Bromodeoxyuridine - metabolism;Catechin - analogs & derivatives;Catechin - pharmacology;Cell Proliferation - drug effects;Cells, Cultured;Chromones - pharmacology;Humans;MAP Kinase Signaling System - drug effects;Morpholines - pharmacology;p38 Mitogen-Activated Protein Kinases - metabolism;Phosphatidylinositol 3-Kinases - metabolism;Phosphorylation - drug effects;Proto-Oncogene Proteins c-akt - metabolism;Tea - chemistry;Trophoblasts - drug effects;Trophoblasts - metabolism
    日期: 2016-08-01
    上傳時間: 2026-04-23 11:12:57 (UTC+8)
    出版者: American Physiological Society;United States
    摘要: 摘要: Green tea catechins, especially (−)-epigallocatechin gallate (EGCG), have been reported to circulate in the placenta of animals and blood of humans after consumption. Whether EGCG regulates activity of human villous trophoblasts (HVT) is unknown. This study investigated the pathways involved in EGCG modulation of trophoblast mitogenesis. EGCG inhibited trophoblast proliferation in a dose-dependent and time-dependent manner, as indicated by the number of cells and incorporation of bromodeoxyuridine (BrdU). EGCG was more effective than other green tea catechins in inhibiting cell growth. EGCG also increased the phosphorylation of the MAPK pathway proteins, ERK1/2, and p38, but not JNK. Furthermore, EGCG had no effects on the total amounts of ERK1/2, p38 MAPK, and JNK proteins. This suggests that EGCG selectively affects particular MAPK subfamilies. Pretreatment with specific inhibitors of ERK1/2, p38 MAPK, and AMP-activated protein kinase (AMPK) antagonized EGCG-induced decreases in both cell number and BrdU incorporation. These inhibitors also blocked EGCG-induced increases in the levels of phospho-ERK1/2, phospho-p38, and phospho-AMPK proteins, respectively. Moreover, EGCG was similar to the phosphatidylinositol 3-kinase inhibitors wortmannin and LY-294002 to decrease protein kinase B (AKT) phosphorylation, cell number, and BrdU incorporation. These data imply that EGCG inhibits the growth of HVT through the ERK, p38, AMPK, and AKT pathways.
    其他題名: Am J Physiol Cell Physiol
    出版者: United States
    出版日期: 2016-08-01
    出處: American Journal of Physiology: Cell Physiology, 2016-08, Vol.311 (2), p.C308-C321
    版權: Copyright © 2016 the American Physiological Society.
    識別號: ISSN: 0363-6143
    識別號: ISSN: 1522-1563
    識別號: EISSN: 1522-1563
    識別號: DOI: 10.1152/ajpcell.00003.2016
    識別號: PMID: 27147558
    顯示於類別:[生命科學系] 期刊論文

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