Anti-angiogenic effects of green tea catechin on an experimental endometriosis mouse model

Hui Xu, H Xu, Wai Ting Lui, W T Lui, Ching Yan Chu, C Y Chu, P S Ng, Pak-yiu Ng, C C Wang, Chi Chiu Wang, M S Rogers, Michael S. Rogers
Human Reproduction · 2008 · vol. 24(3) , pp. 608–618 · doi:10.1093/humrep/den417 · PMID:19088106 · W2138971616
article OA: bronze CC0 ⤵ 60 in-corpus citations
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Green tea catechin EGCG significantly reduced the size and microvessel density of experimental endometriosis lesions by inhibiting angiogenesis and inducing apoptosis.

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Abstract

BACKGROUND: The development of new blood vessels plays an essential role in growth and survival of endometriosis. Epigallocatechin gallate (EGCG) from green tea has powerful anti-angiogenic properties and our aim was to evaluate these properties in experimental endometriosis. METHODS AND RESULTS: Eutopic endometrium from endometriosis patients was transplanted s.c. to severely compromised immunodeficient mice, randomly treated i.p. with EGCG (anti-angiogenic and -oxidant), Vitamin E (a non-angiogenic antioxidant) or saline for 2 weeks. The endometrial implant, including adjacent host outer skin and subcutaneous layers plus inner abdominal muscle and peritoneum, was collected. New microvessels were determined by species-specific immunohistochemistry. Angiogenic factors in lesions and abdominal muscle were detected by quantitative real-time PCR. Apoptosis was studied by terminal deoxynucleotidyltransferase-mediated dUTP nick-end labelling and quantitative real-time PCR. In saline control, endometrial implants developed new blood vessels with proliferating glandular epithelium and were tightly adhered to host subcutaneous and abdominal muscle layers. After EGCG, endometriotic lesions were smaller than control (P < 0.05), and glandular epithelium was smaller and eccentrically distributed. Angiogenesis in lesions from the implant and adjacent tissues was under-developed, and microvessel size and density were lower (both P < 0.01) than control. mRNA for angiogenic vascular endothelial growth factor A, but not hypoxia inducible factor 1, alpha subunit, was significantly down-regulated in lesions after EGCG (P < 0.05). In addition, apoptosis in the lesions was more obvious, and nuclear factor kappa B and mitogen activated protein kinase 1 mRNA levels were up-regulated (P < 0.05) after EGCG treatment. No differences were observed with Vitamin E treatment. CONCLUSIONS: EGCG significantly inhibits the development of experimental endometriosis through anti-angiogenic effects.

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Condition tags

mesh:D004715endometriosis

MeSH descriptors

Angiogenesis Inhibitors Catechin Endometriosis Angiogenesis Inhibitors Animals Catechin Cell Proliferation Disease Models, Animal Endometriosis Endometriosis Endometriosis Endometrium Endometrium Female Humans Mice Mice, SCID Microcirculation Neovascularization, Pathologic Tea

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