中文摘要：

ObjectiveThis 学习试图调查表达式模式和原子受体亚科 2 组 E 成员的功能( Nr2e1 ) 1 在 retinoic 酸( RA )劝诱了大脑反常的大脑 abnormality.MethodsThe 鼠标模型被管理 28 mg/kg RA 建立，并且神经干细胞( NSC )从鼠标胚胎被孤立并且在 vitro 有教养。Nr2e1 表示被整个山在 situ 杂交， RT-PCR，并且西方的弄污检测。Nr2e1 功能被 transducing Nr2e1 shRNA 在表明小径的声音的刺猬(嘘) 上决定进 NSC，和效果在房间被估计。另外，由 RA 的表示也是的 Nr2e1 的规定在 vitro.ResultsNr2e1 决定表示是显著地在对待 RA 的老鼠胚胎的大脑和 NSC 的 downregulated，并且影响的 Nr2e1 击倒在 vitro 的 NSC 的增长。另外，在有 RA.ConclusionOur 学习的不同集中的 NSC 的处理证明 Nr2e1 能被 RA 调整以后， Nr2e1 的一个类似的表示模式和 RA 受体(RAR ) 被观察，它将帮助位于导致 RA 的大脑反常下面的机制的更好的理解。

英文摘要：

Objective This study aimed to investigate the expression pattern and function of Nuclear receptor subfamily 2 group E member 1 （Nr2e1） in retinoic acid （RA）-induced brain abnormality. Methods The mouse model of brain abnormality was established by administering 28 mg/kg RA, and neural stem cells （NSCs） were isolated from the mouse embryo and cultured in vitro. Nr2e1 expression was detected by whole mount in situ hybridization, RT-PCR, and Western blotting. Nr2e1 function was determined by transducing Nr2e1 sh RNA into NSCs, and the effect on the sonic hedgehog （Shh） signaling pathway was assessed in the cells. In addition, the regulation of Nr2e1 expression by RA was also determined in vitro. Results Nr2e1 expression was significantly downregulated in the brain and NSCs of RA-treated mouse embryos, and knockdown of Nr2e1 affected the proliferation of NSCs in vitro. In addition, a similar expression pattern of Nr2e1 and RA receptor （RAR） α was observed after treatment of NSCs with different concentrations of RA. Conclusion Our study demonstrated that Nr2e1 could be regulated by RA, which would aid a better understanding of the mechanism underlying RA-induced brain abnormality.