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植物雌激素染料木黄酮对雌二醇诱导的子宫肌瘤细胞增殖的抑制作用。

Repressive effect of the phytoestrogen genistein on estradiol-induced uterine leiomyoma cell proliferation.

机构信息

Center for Asian Traditional Medicine, Tohoku University Graduate School of Medicine, Aoba, Sendai 980-8574, Japan.

出版信息

Gynecol Endocrinol. 2009 Jun;25(6):403-9. doi: 10.1080/09513590902730804.

DOI:10.1080/09513590902730804
PMID:19903033
Abstract

OBJECTIVE

Uterine leiomyomas are the most common gynecological benign tumor and greatly affect reproductive health and well-being. They are the predominant indication for hysterectomy in premenopausal women. Current epidemiological study reported that soy products intake is inversely associated with diseases leading to hysterectomy. Genistein is a soy-derived phytoestrogen and its inhibitory effect on leiomyoma cell proliferation is reported. In this study, we investigated the siginificant inhibitory effect of genistein on estradiol (E(2))-induced leiomyoma cells proliferation.

STUDY DESIGN

The Eker rat-derived uterine leiomyoma cell line ELT-3 cells were used. Cell proliferation was assessed by counting the number of cells. The expression of estrogen receptors and peroxisome proliferator-activated receptor-gamma (PPARgamma) was evaluated by Western blot analysis.

RESULTS

PPARgamma was expressed in ELT-3 cells and genistein acted as PPARgamma ligand. This inhibitory effect of genistein was attenuated by the treatment of cells with PPARgamma antagonist bisphenol A diglycidyl ether (BADGE) or GW9662.

CONCLUSION

These experimental findings in vitro show that the repressive effect of genistein on E(2)-induced ELT-3 cell proliferation is through the activation of PPARgamma. Genistein may be useful as an alternative therapy for leiomyoma.

摘要

目的

子宫肌瘤是最常见的妇科良性肿瘤,严重影响生殖健康和生活质量。它是绝经前妇女行子宫切除术的主要指征。目前的流行病学研究报告称,大豆制品的摄入与导致子宫切除术的疾病呈负相关。染料木黄酮是一种大豆来源的植物雌激素,其对子宫肌瘤细胞增殖的抑制作用已有报道。在这项研究中,我们研究了染料木黄酮对雌二醇(E(2))诱导的子宫肌瘤细胞增殖的显著抑制作用。

研究设计

使用 Eker 大鼠来源的子宫肌瘤细胞系 ELT-3 细胞。通过计数细胞数量来评估细胞增殖。通过 Western blot 分析评估雌激素受体和过氧化物酶体增殖物激活受体-γ(PPARγ)的表达。

结果

PPARγ在 ELT-3 细胞中表达,染料木黄酮作为 PPARγ配体。用 PPARγ拮抗剂双酚 A 二缩水甘油醚(BADGE)或 GW9662 处理细胞可减弱染料木黄酮的这种抑制作用。

结论

这些体外实验结果表明,染料木黄酮对 E(2)诱导的 ELT-3 细胞增殖的抑制作用是通过激活 PPARγ 实现的。染料木黄酮可能可作为子宫肌瘤的一种替代疗法。

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