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Puerarin Suppresses Invasion and Vascularization of Endometriosis Tissue Stimulated by 17ß-Estradiol
Published: Thursday, September 15, 2011
Author: Dan Wang et al.

by Dan Wang, Yuhuan Liu, Jie Han, Dongxia Zai, Mei Ji, Wen Cheng, Ling Xu, Luxi Yang, Miaoxia He, Jian Ni, Zailong Cai, Chaoqin Yu


Puerarin, a phytoestrogen with a weak estrogenic effect, binds to estrogen receptors, thereby competing with 17ß-estradiol (E2) and producing an anti-estrogenic effect. This study was to investigate whether puerarin could suppress the invasion and vascularization of E2-stimulated endometriotic tissue.

Methodology/Principal Findings

The endometriotic stromal cells (ESCs) were successfully established and their invasive ability under different treatments was assessed through a Transwell Assay. Simultaneously, matrix metallopeptidase 9 (MMP-9) and tissue inhibitor of metalloproteinase 1 (TIMP-1) were detected by western blotting. Vascularization of endometriotic tissues was observed by chicken chorioallantoic membrane (CAM) assay. The staining of MMP-9, intercellular adhesion molecule 1 (ICAM-1), TIMP-1, and vascular endothelial growth factor (VEGF) in grafted endometriotic tissues was examined using immunohistochemistry analysis. The purity of ESCs in isolated cells was >95%, as determined by the fluoroimmunoassay of vimentin. E2 (10-8 mol/L) promoted the invasiveness of ESCs by increasing MMP-9 accumulation and decreasing TIMP-1 accumulation. Interestingly, puerarin (10-9 mol/L) significantly reversed these effects (P<0.01). The CAM assay indicated that puerarin (10-9 mol/L) also inhibited the angiopoiesis of endometriotic tissue stimulated by the E2 (10-8 mol/L) treatment (P<0.05). Accordingly, immunohistochemistry showed that the accumulation of MMP-9, ICAM-1, and VEGF was reduced whereas that of TIMP-1 increased in the combination treatment group compared with the E2 treatment group.


This study demonstrated that puerarin could suppress the tissue invasion by ESCs and the vascularization of ectopic endometrial tissues stimulated by E2, suggesting that puerarin may be a potential drug for the treatment of endometriosis.