Expression of vascular endothelial growth factor C and anti-angiogenesis therapy in endometriosis.

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VEGF-C expression is higher in endometriosis tissues and correlates with disease severity, and Endostar treatment significantly reduces endometriotic implants and VEGF-C expression in a rat model.

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Abstract

Angiogenesis is an important pathogenesis of Endometriosis. Vascular endothelial growth factor C (VEGF-C) is one of the most important factor in the regulation of both normal and abnormal angiogenesis. Anti-angiogenic treatment of endometriosis is still in the exploratory stage. In this study, we investigate the relationship between VEGF-C and endometriosis, the therapeutic effects of Endostar in the rat endometriosis model. We then demonstrated that Immunohistochemical expression of VEGF-C was higher in endometriotic tissues than in control normal ovary tissues (P < 0.01) and higher in the endomertriosis grade III-IV than in endomertriosis grade I-II (P=0.013). In rat endometriosis model, we observed a significant reduction in the mean volume and weight of the endometriotic implants per rat in the treatment group as compared with the control group. By immunohistochemical evaluation, there was a significant reduction in VEGF-C expression after treatment in all areas examined. VEGF-C may be involved in the pathogenesis of endomertriosis by regulating the angiogenesis. Endostar has therapeutic effects of endometriosis lesions in the rat endometriosis model.

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Condition tags

endometriosis

MeSH descriptors

Endometriosis Endometrium Neovascularization, Pathologic Vascular Endothelial Growth Factor C Adult Animals Disease Models, Animal Endometriosis Endometriosis Endometriosis Endometrium Endometrium Endometrium Endostatins Endostatins Endostatins Female Humans Middle Aged Neovascularization, Pathologic

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