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Hum. Reprod. Advance Access originally published online on July 4, 2008
Human Reproduction 2008 23(10):2308-2318; doi:10.1093/humrep/den245
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© The Author 2008. Published by Oxford University Press on behalf of the European Society of Human Reproduction and Embryology. All rights reserved. For Permissions, please email: journals.permissions@oxfordjournals.org

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

Matthias W. Laschke1,3, Christine Schwender1, Claudia Scheuer1, Brigitte Vollmar2 and Michael D. Menger1

1 Institute for Clinical and Experimental Surgery, University of Saarland, D-66421 Homburg/Saar, Germany 2 Institute for Experimental Surgery, University of Rostock, Schillingallee 69a, 18055 Rostock, Germany

3 Correspondence address. Tel: +49-6841-162-6554; Fax: +49-6841-162-6553; E-mail: matthias.laschke{at}uniklinik-saarland.de

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 (E2), 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 E2-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.

Key words: epigallocatechin-3-gallate/green tea/endometriosis/angiogenesis/intravital fluorescence microscopy

Submitted on April 15, 2008; resubmitted on May 26, 2008; accepted on June 2, 2008.


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