目的 建立肾虚型子宫内膜容受障碍大鼠模型，探讨其容受障碍的免疫学机制。方法 以羟基脲建立肾虚型大鼠模型，比较模型大鼠与正常雌性大鼠动情期外周血自然杀伤（NK）细胞CD56⁺CD16⁺、CD56⁺CD16^?、CD56^?CD16⁺亚群水平，白细胞介素-2（IL-2）、白血病抑制因子（LIF）水平，以及内膜IL-2、LIF、各亚群NK细胞表达。大鼠羟基脲造模后妊娠第11天，比较其与正常妊娠大鼠外周血NK细胞、IL-2和LIF的量，以及蜕膜中IL-2、LIF、各亚群NK细胞表达。结果 模型组大鼠外周血CD56^?CD16⁺较正常大鼠明显增加、CD56⁺CD16^?/CD56^?CD16⁺明显减少（P＜0.05）；内膜CD56⁺CD16⁺、CD56⁺CD16^?均明显减少（P＜0.05），LIF明显减少（P＜0.05）；造模大鼠妊娠后，蜕膜LIF较正常妊娠大鼠明显减少（P＜0.05）。结论 羟基脲致肾虚型大鼠模型子宫内膜容受障碍，其致病机制是全身和局部免疫功能异常，可影响妊娠结局。

Objective To establish the model of endometrial receptivity disorder in kidney deficiency rats and to explore the immunological mechanism. Methods The model of kidney deficiency rats was established using hydroxyl urea. We measured the quantities of natrual killer (NK) cells, CD56⁺CD16⁺, CD56⁺CD16^?, CD56^?CD16⁺ subsets, IL-2, LIF in peripheral blood, and expression of IL-2, LIF, and NK cells of all subgroups in endometriums of model and normal rats in their estrous cycles. We also observed the changes of IL-2, LIF, and NK cells of all subgroups in both peripheral blood and decidua on day 11 of pregnancy. Results Compared with the control group, the CD56^?CD56⁺ level was increased and CD56⁺CD16^?/CD56^?CD16⁺ level was decreased in peripheral blood (P<0.05); The levels of CD56⁺CD16⁺ and CD56⁺CD16^? and the content of LIF were obviously decreased in endometriums (P<0.05). LIF in decidua of pregnant rats was lower than that in normal rats (P<0.05). Conclusion Hydroxyuea can imitate the kidney deficiency in rats with endometrial receptivity disorder. The possible mechanism may be related to abnormal immune system changes. Pregnancy outcome may as well be impacted.

广东省教育厅普通高校重点实验室开放基金（ZF201115）