title: Epigallocatechin-3-gallate inhibits estrogen-induced activation of endometrial cells in vitro and causes regression of endometriotic lesions in vivo.
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.
authors.affiliation: Institute for Clinical and Experimental Surgery, University of Saarland, Homburg, Saar, Germany. matthias.laschke@uniklinik-saarland.de
authors.forename: Matthias W
authors.initials: MW
authors.lastname: Laschke
authors.forename: Christine
authors.initials: C
authors.lastname: Schwender
authors.forename: Claudia
authors.initials: C
authors.lastname: Scheuer
authors.forename: Brigitte
authors.initials: B
authors.lastname: Vollmar
authors.forename: Michael D
authors.initials: MD
authors.lastname: Menger
mesh_terms: D020533:Angiogenesis Inhibitors / Q000494:pharmacology* / Q000627:therapeutic use; D000818:Animals; D002392:Catechin / Q000031:analogs & derivatives* / Q000494:pharmacology / Q000627:therapeutic use; D002460:Cell Line; D049109:Cell Proliferation / Q000187:drug effects; D006224:Cricetinae; D004715:Endometriosis / Q000188:drug therapy* / Q000473:pathology; D004717:Endometrium / Q000187:drug effects / Q000473:pathology; D004958:Estradiol / Q000502:physiology; D005260:Female; D015870:Gene Expression / Q000187:drug effects; D006080:Ovarian Follicle / Q000098:blood supply / Q000187:drug effects; D042461:Vascular Endothelial Growth Factor A / Q000378:metabolism
chemical_list: D020533:Angiogenesis Inhibitors; D042461:Vascular Endothelial Growth Factor A; D004958:Estradiol; D002392:Catechin; C045651:epigallocatechin gallate