白细胞介素1受体Ⅱ型在子宫内膜异位症发生机制中的作用

Roles of Interleukin-1 Receptor Type II in the Pathogenesis of Endometriosis

目的:研究白细胞介素1受体II型(IL-1RII)在子宫内膜异位症(EMs)发生机制中的作用。方法:体外培养子宫内膜细胞经过可溶性IL-1RII或IL-1RII重组腺病毒(rAd-RII)作用12h后收集细胞培养液,酶联免疫吸附试验(ELISA)检测细胞培养液中IL-6和IL-8的水平。另外应用二维电泳和质谱分析鉴定rAd-RII作用后的差异表达蛋白。结果:2.0μg/mL的可溶性IL-1RII显著抑制了内膜细胞IL-6和IL-8的分泌。rAd-RII感染内膜细胞后IL-1β刺激IL-8的分泌比磷酸盐缓冲液(PBS)和LacZ重组腺病毒(rAd-LacZ)对照组显著降低,而IL-6表达无显著差异。二维电泳分析有62个差异蛋白点,质谱分析鉴定出34个差异蛋白,大多数蛋白和细胞代谢与增殖相关。结论:IL-1RII能阻断IL-1β对内膜基质细胞的作用,可能为EMs治疗提供新策略。

Objective：To investigate the roles of Interleukin-1 receptor type Ⅱ （IL-1RⅡ） in the pathogenesis of endometriosis. Methods： Endometrial cells cultured in vitro were exposed to soluble IL-1RⅡ or the recombinant adenovirus of IL-IRⅡ （rAd-RⅡ） for 12 hours, and then cell culture media were collected. The levels of IL-6 and IL-8 in the culture media were measured via enzyme-linked immunosorbent assay （ELISA）, and the differential expression proteins were identified by two-dimensional electrophoresis and MALDI-TOF mass spectrometry after rAd-RII exposure. Results： Soluble IL-1RⅡ （2.0 ug/ml） significantly inhibited the secretion of IL-6 and IL-8 in endometrial cells. The secretion of IL-8 induced by IL-1β in endometrial cells infected with rAd- RⅡ was significantly lower than the PBS and rAd-LacZ control groups, while there were no significant differences of IL-6 secretion. 62 spots of differential expression proteins were collected through two-dimensional electrophoresis and 34 differential expression proteins were identified by MALDI-TOF mass spectrometry. The majority of these identified proteins were related to cellular metabolism and proliferation. Conclusion： These results suggest that IL- 1RⅡ can counteract the effects of IL-1β on endometrial stromal cells and may provide a new clinical strategy for the treatment of endometriosis.