Abstract
BackgroundPuerarin, a phytoestrogen with a weak estrogenic effect, binds to estrogen receptors, thereby competing with 17β-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 FindingsThe 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.Conclusions/SignificanceThis 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.
Highlights
Endometriosis, a common, benign, estrogen-dependent disease affecting 3%–10% of women of reproductive age, is defined as the presence of endometrial glands and stroma outside of the uterine cavity [1]
Conclusions/Significance: This study demonstrated that puerarin could suppress the tissue invasion by endometriotic stromal cells (ESCs) and the vascularization of ectopic endometrial tissues stimulated by E2, suggesting that puerarin may be a potential drug for the treatment of endometriosis
The key enzymes that regulate the extracellular matrix (ECM) are the matrix metalloproteinases (MMPs), and peritoneal invasion by endometrial tissue is thought to be dependent on MMPs and their corresponding tissue inhibitors of metalloproteinases (TIMPs)
Summary
Endometriosis, a common, benign, estrogen-dependent disease affecting 3%–10% of women of reproductive age, is defined as the presence of endometrial glands and stroma outside of the uterine cavity [1]. It is not a malignant disorder but it has similarities to a developing tumor. The initial phase of endometriosis is an invasive event that requires extracellular matrix (ECM) breakdown. The key enzymes that regulate the ECM are the matrix metalloproteinases (MMPs), and peritoneal invasion by endometrial tissue is thought to be dependent on MMPs and their corresponding tissue inhibitors of metalloproteinases (TIMPs). This study was to investigate whether puerarin could suppress the invasion and vascularization of E2-stimulated endometriotic tissue
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