目的 建立腎虛型子宮內(nèi)膜容受障礙大鼠模型，探討其容受障礙的免疫學機制。方法 以羥基脲建立腎虛型大鼠模型，比較模型大鼠與正常雌性大鼠動情期外周血自然殺傷（NK）細胞CD56⁺CD16⁺、CD56⁺CD16^?、CD56^?CD16⁺亞群水平，白細胞介素-2（IL-2）、白血病抑制因子（LIF）水平，以及內(nèi)膜IL-2、LIF、各亞群NK細胞表達。大鼠羥基脲造模后妊娠第11天，比較其與正常妊娠大鼠外周血NK細胞、IL-2和LIF的量，以及蛻膜中IL-2、LIF、各亞群NK細胞表達。結果 模型組大鼠外周血CD56^?CD16⁺較正常大鼠明顯增加、CD56⁺CD16^?/CD56^?CD16⁺明顯減少（P＜0.05）；內(nèi)膜CD56⁺CD16⁺、CD56⁺CD16^?均明顯減少（P＜0.05），LIF明顯減少（P＜0.05）；造模大鼠妊娠后，蛻膜LIF較正常妊娠大鼠明顯減少（P＜0.05）。結論 羥基脲致腎虛型大鼠模型子宮內(nèi)膜容受障礙，其致病機制是全身和局部免疫功能異常，可影響妊娠結局。

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.

廣東省教育廳普通高校重點實驗室開放基金（ZF201115）