摘要
目的:探讨可溶性IL-1Ⅱ型受体(sIL-1RⅡ)对人白细胞介素1α(IL-1α)诱导子宫内膜异位症(EMs)在位内膜基质细胞(ESC)表达白细胞介素8(IL-8)的影响。方法:体外培养EMs在位内膜基质细胞,分别以含不同浓度IL-1α(0、0.1、1.0、10、100ng/ml)的DMEM/F12培养基孵育24h,利用RT-PCR和ELISA法从转录和蛋白翻译水平分别检测IL-8的表达情况。选取能显著刺激IL-8升高的IL-1α浓度,作用于EMs在位内膜基质细胞不同时间,RT-PCR和ELISA法检测IL-8的表达情况。并检测1.0μg/ml的sIL-1RⅡ对不同浓度IL-1α诱导EMs在位内膜基质细胞表达IL-8的影响。结果:未刺激时,EMs在位内膜基质细胞能表达低水平IL-8,经IL-1α刺激后IL-8mRNA及蛋白表达均升高,并呈剂量和时间依赖性,差异有统计学意义(P<0.01)。1.0μg/mlsIL-1RⅡ能拮抗低浓度IL-1α的刺激效应。结论:IL-1α能以时间剂量依赖方式刺激EMs在位内膜基质细胞表达IL-8,促进EMs的发生发展,sIL-1RⅡ能一定程度拮抗此作用,为EMs的生物治疗提供了理论基础。
Objective:To explore the effects of soluble intedeukin-1 receptor type Ⅱ (sIL-1RⅡ)on intedeukin-1α(IL-1α)-induced expression of IL-8 in eutopic endometrial stromal'cells (ESC) from patients with endometriosis (EMs). Methods:ESC from patients with EMs were cultured in vitro. Stromal cells were treated with different concentrations of IL-1α (0,0.1,1.0,10,100 ng/ml) respectively for 24 h. Enzyme-linked immuno-assay (ELISA) and RT-PCR were used to examine the expression of IL-8 in transcriptional and translational levels. The concentration of IL-1α which could remarkably enhance the expression of IL-8 was used to stimulate ESC for different times. The levels of IL-8 were measured at each time point by RT-PCR and ELISA. Meanwhile, the effects of 1.0 μg/ml of sIL-1R Ⅱ on IL-1α-induced expression of IL-8 were detected. Resuits:ESC could slightly express IL-8 without stimulation. The levels of IL-8 protein and mRNA were both remarkably increased after IL-1α stimulation in a dose- and time- dependent manner. IL-8 expression induced by low concentration of IL-1α was inhibited by 1.0 μg/rnl sIL-1R Ⅱ. Conclusion:IL-1α can induce IL-8 expression in eutopic ESC of EMs in a dose- and time-dependent manner. It may contribute to the pathogenesis and development of EMs. sIL-1R Ⅱ can partially antagonize the effect of IL-1α and may offer a rational therapy method for endometriosis.
出处
《南京医科大学学报(自然科学版)》
CAS
CSCD
北大核心
2007年第4期307-311,共5页
Journal of Nanjing Medical University(Natural Sciences)
基金
国家自然科学基金资助项目(781ba0612)
江苏省自然科学基金创新人才启动基金资助项目(781da0603)
江苏省135医学重点学科苏教卫[2003]19