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

详细信息    查看全文

• 作者：Aiping Qin^a ; ¹ ; ^{apqin2001@sina.com" class="auth_mail" title="E-mail the corresponding author} ; Jinchun Qin^a ; ¹ ; Yufu Jin^a ; Wei Xie^a ; Li Fan^b ; Lingyun Jiang^a ; Fuhua Mo^a
• 关键词：Dehydroepiandrosterone ; Endometrial stromal cells ; Endometrium ; Androgen receptor
• 刊名：European Journal of Obstetrics & Gynecology and Reproductive Biology
• 出版年：2016
• 出版时间：March 2016
• 年：2016
• 卷：198
• 期：Complete
• 页码：120-126
• 全文大小：1334 K

文摘

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 100 nM. However, DHEA (100 nM) 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.