Green tea (-)-epigallocatechin gallate inhibits the growth of human villous trophoblasts via the ERK, p38, AMP-activated protein kinase, and AKT pathways.

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 pERK1/2, pp38, and pAMPK proteins, respectively. Moreover, EGCG was similar to the PI3K inhibitors wortmannin and LY294002 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.
PMID: 27147558 [PubMed - as supplied by publisher]

Source: Am J Physiol Cell Ph... - May 3, 2016 Category: Cytology Authors: Shih LJ, Chen TF, Lin CK, Liu HS, Kao YH Tags: Am J Physiol Cell Physiol Source Type: research