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脱氢表雄酮可提高子宫内膜基质细胞的抗氧化能力,并通过雄激素受体改善子宫内膜容受性。

DHEA improves the antioxidant capacity of endometrial stromal cells and improves endometrium receptivity via androgen receptor.

作者信息

Qin Aiping, Qin Jinchun, Jin Yufu, Xie Wei, Fan Li, Jiang Lingyun, Mo Fuhua

机构信息

Department of Reproductive Center, First Affiliated Hospital of Guangxi Medical University, Nanning, Guangxi Zhuang Autonomous Region, China.

Department of Reproductive Center, First Affiliated Hospital of Guangxi Medical University, Nanning, Guangxi Zhuang Autonomous Region, China.

出版信息

Eur J Obstet Gynecol Reprod Biol. 2016 Mar;198:120-126. doi: 10.1016/j.ejogrb.2016.01.016. Epub 2016 Jan 15.

DOI:10.1016/j.ejogrb.2016.01.016
PMID:26835588
Abstract

OBJECTIVE

To investigate the effect of dehydroepiandrosterone (DHEA) on mouse decidual endometrial stromal cells (ESCs) and to explore mechanisms regulating endometrial receptivity.

STUDY DESIGN

Mouse ESCs were incubated with increasing concentrations of DHEA during decidualization. Treatment with flutamide (FLU), a specific androgen receptor (AR) antagonist, was also performed. Flow cytometry was used to measure intracellular reactive oxygen species (ROS). Real time-PCR was used to determine mRNA expression of decidual PRL-related protein (dPRP), AR, and HomeoboxA10 (HOXA10). Protein levels of AR and HOXA10 were measured by western blot.

RESULTS

DHEA significantly inhibited ESC proliferation at concentrations ≥1×10(-6)M. DHEA treatment reduced intracellular ROS in a dose-dependent manner. Expression of dPRP was minimally affected by DHEA at concentrations of 1 to 100nM. However, DHEA (100nM) significantly increased the expression of HOXA10 at both the mRNA and protein levels (P<0.01). Importantly, this DHEA-mediated increase in HOXA10 was attenuated by treatment with FLU. Finally, neither DHEA nor FLU influenced expression of AR mRNA or protein.

CONCLUSION

Low concentration of DHEA improves the antioxidant capacity of decidual ESCs. DHEA treatment may also improve endometrium receptivity via AR.

摘要

目的

研究脱氢表雄酮(DHEA)对小鼠蜕膜化子宫内膜基质细胞(ESCs)的影响,并探讨调节子宫内膜容受性的机制。

研究设计

在蜕膜化过程中,将小鼠ESCs与浓度递增的DHEA一起孵育。还使用了氟他胺(FLU),一种特异性雄激素受体(AR)拮抗剂进行处理。采用流式细胞术测量细胞内活性氧(ROS)。使用实时定量聚合酶链反应(Real time-PCR)测定蜕膜催乳素相关蛋白(dPRP)、AR和同源框A10(HOXA10)的mRNA表达。通过蛋白质印迹法测量AR和HOXA10的蛋白质水平。

结果

当浓度≥1×10⁻⁶M时,DHEA显著抑制ESCs增殖。DHEA处理以剂量依赖的方式降低细胞内ROS。在1至100nM浓度下,DHEA对dPRP表达的影响最小。然而,DHEA(100nM)在mRNA和蛋白质水平上均显著增加HOXA10的表达(P<0.01)。重要的是,FLU处理减弱了DHEA介导的HOXA10增加。最后,DHEA和FLU均未影响AR mRNA或蛋白质的表达。

结论

低浓度的DHEA可提高蜕膜化ESCs的抗氧化能力。DHEA处理也可能通过AR改善子宫内膜容受性。

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