uNK细胞在绝经后激素补充治疗期间子宫异常出血中的作用

Role of uNK cells in postmenopausal abnormal uterine bleeding during hormone replacement therapy

目的探讨绝经后激素补充治疗(替勃龙)期间子宫异常出血中子宫自然杀伤细胞(uNK细胞)的表达及可能作用机制。方法采用免疫组化检测绝经后采用替勃龙治疗者发生子宫异常出血(n=29)与非治疗者发生出血(n=31)时内膜组织中uNK细胞(CD56+细胞)表达及其与VEGF及Ang-2的关系。结果治疗组和非治疗组子宫内膜组织中uNK细胞计数分别为67.49±7.52和33.67±7.44,差异具有统计学意义(P<0.05);治疗组VEGF和Ang-2阳性表达率、过表达率均高于非治疗组,差异均具有统计学意义(P<0.05)。uNK细胞与VEGF、Ang-2的表达均呈正相关(P<0.05)。结论绝经后替勃龙治疗可能通过诱导内膜组织中uNK细胞的聚集,通过促使VEGF和Ang-2分泌增加,进而影响内膜血管的稳定性,从而参与了异常出血的过程。

Objective To explore the role of uNK cell in postmenopausal abnormal endometrial bleeding during tibolone therapy.Methods The endometrial tissues were obtained from 29 patients with abnormal uterine bleeding in tibolone group and 31 patients with abnormal uterine bleeding in non-treatment group.Endometrial CD56 ＋ （uNK cell marker） was determined by immunohistochemistry,and its correlation with VEGF and Ang-2 was analyzed.Results Endometrial CD56 ＋ uNK cell counts,positive rates of VEGF and Ang-2 expression,and the percentages of VEGF and Ang-2 overexpression were significantly higher in tibolone group than those in non-treatment group （P ＜ 0.05）.The CD56 ＋ uNK cells were positively correlated with the VEGF and Ang-2 expression （P ＜ 0.05）.Conclusion The aggregation of uNK cells in endometrium induced by tibolone may promote endometrial hypervascularization likely via secreting VEGF and Ang-2 for decreasing the vascular stability,thereby increasing the abnormal bleeding during postmenopause.