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Hum Reprod. 2008 Oct;23(10):2308-18. doi: 10.1093/humrep/den245. Epub 2008 Jul 4.

Epigallocatechin-3-gallate inhibits estrogen-induced activation of endometrial cells in vitro and causes regression of endometriotic lesions in vivo.

Author information

1
Institute for Clinical and Experimental Surgery, University of Saarland, Homburg, Saar, Germany. matthias.laschke@uniklinik-saarland.de

Abstract

BACKGROUND:

Epigallocatechin-3-gallate (EGCG), the major component of green tea, is a pleiotropic substance, which may inhibit tumor growth via multiple intracellular signaling pathways. Herein, we studied whether EGCG may also be effective in the treatment of endometriosis.

METHODS:

We investigated the effect of EGCG on activation by estradiol (E(2)), proliferation and vascular endothelial growth factor (VEGF) expression of isolated hamster endometrial stromal cells and glandular cells in vitro using the water-soluble tetrazolium (WST)-1 colorimetric assay and western blot analysis. In the dorsal skinfold chamber model of Syrian golden hamsters, which were treated for 14 days with EGCG or vehicle, we further analyzed angiogenesis, blood perfusion and tissue integrity of both endometriotic lesions and ovarian follicles by intravital fluorescence microscopy and histology.

RESULTS:

We found that EGCG suppresses E(2)-stimulated activation, proliferation and VEGF expression of endometrial cells in vitro (all P < 0.05). Furthermore, EGCG selectively inhibited angiogenesis and blood perfusion (P < 0.05) of endometriotic lesions in vivo without affecting blood vessel development in ovarian follicles. Histology confirmed that EGCG-treatment induces regression of the endometriotic lesions.

CONCLUSIONS:

Our data indicate that EGCG might be a promising therapeutic agent in the treatment of endometriosis, preventing the establishment of new endometriotic lesions.

PMID:
18603648
DOI:
10.1093/humrep/den245
[Indexed for MEDLINE]

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