Puerarin suppresses invasion and vascularization of endometriosis tissue stimulated by 17β-estradiol.

BACKGROUND: Puerarin, 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 endomet...

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Main Authors: Dan Wang, Yuhuan Liu, Jie Han, Dongxia Zai, Mei Ji, Wen Cheng, Ling Xu, Luxi Yang, Miaoxia He, Jian Ni, Zailong Cai, Chaoqin Yu
Format: Article
Language:English
Published: Public Library of Science (PLoS) 2011-01-01
Series:PLoS ONE
Online Access:http://europepmc.org/articles/PMC3174250?pdf=render
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author Dan Wang
Yuhuan Liu
Jie Han
Dongxia Zai
Mei Ji
Wen Cheng
Ling Xu
Luxi Yang
Miaoxia He
Jian Ni
Zailong Cai
Chaoqin Yu
author_facet Dan Wang
Yuhuan Liu
Jie Han
Dongxia Zai
Mei Ji
Wen Cheng
Ling Xu
Luxi Yang
Miaoxia He
Jian Ni
Zailong Cai
Chaoqin Yu
author_sort Dan Wang
collection DOAJ
description BACKGROUND: Puerarin, 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 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. CONCLUSIONS/SIGNIFICANCE: 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.
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spelling doaj.art-d1fbe509f88f4bc9ab541692c6370b822022-12-22T03:04:09ZengPublic Library of Science (PLoS)PLoS ONE1932-62032011-01-0169e2501110.1371/journal.pone.0025011Puerarin suppresses invasion and vascularization of endometriosis tissue stimulated by 17β-estradiol.Dan WangYuhuan LiuJie HanDongxia ZaiMei JiWen ChengLing XuLuxi YangMiaoxia HeJian NiZailong CaiChaoqin YuBACKGROUND: Puerarin, 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 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. CONCLUSIONS/SIGNIFICANCE: 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.http://europepmc.org/articles/PMC3174250?pdf=render
spellingShingle 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 suppresses invasion and vascularization of endometriosis tissue stimulated by 17β-estradiol.
PLoS ONE
title Puerarin suppresses invasion and vascularization of endometriosis tissue stimulated by 17β-estradiol.
title_full Puerarin suppresses invasion and vascularization of endometriosis tissue stimulated by 17β-estradiol.
title_fullStr Puerarin suppresses invasion and vascularization of endometriosis tissue stimulated by 17β-estradiol.
title_full_unstemmed Puerarin suppresses invasion and vascularization of endometriosis tissue stimulated by 17β-estradiol.
title_short Puerarin suppresses invasion and vascularization of endometriosis tissue stimulated by 17β-estradiol.
title_sort puerarin suppresses invasion and vascularization of endometriosis tissue stimulated by 17β estradiol
url http://europepmc.org/articles/PMC3174250?pdf=render
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