摘要
目的:检测艾拉莫德(T-614)对类风湿关节炎(RA)外周血单个核细胞(PBMC)诱导凋亡作用及IL-8细胞因子水平变化,探讨T-614对RA治疗的免疫机制。方法:收集风湿免疫科诊断明确的活动期RA患者,采集全血,处理收集PBMC。制备T-614,使用不同剂量T-614,为高剂量组、中等剂量组和低剂量组与PBMC共培养,孵育1h、3h,通过流式细胞仪检测PBMC凋亡,并收集上清检测IL-8水平。结果:T-614与PBMC共孵育培养,T-614高剂量、中剂量与空白对照组PBMC凋亡率为1h:12.30±2.45%、8.23±2.29%和4.71±2.01%,3h:25.47±4.19%、13.39±3.80%和7.88±2.71%,各组比较使用T-614低剂量,中等剂量与PBMC共孵育培养24h收集上清,ELISA法检测IL-8水平,T-614中、低剂量与空白对照组分别为48.91±8.33μg/ml、125.31±20.02μg/ml和155.36±22.15μg/ml。结论:随着T-614浓度升高,对PBMC细胞凋亡成剂量依赖性趋势,同时降低细胞分泌因子IL-8水平。免疫调控诱导PBMC凋亡、降低趋化因子IL-8水平可能是T-614治疗RA的重要机制。
Objective：To observe the effect of Iguratimod （T‐614） on the apoptosis of peripheral blood mononuclear cells （PBMCs） ,the expression of IL‐8 in rheumatoid arthritis （RA） patients ,and to explore the possi‐ble mechanism of T‐614 in treating RA .Methods ：12 patients were diagnosed with RA referred to the Department of Rheumatology .PBMCs were prepared from 12 patients in active stage of RA and treated with T‐614 at different concentrations （lower dose：5 μg/ml;Moderate dose：50 μg/ml;Higher dose：500μg/ml ） for 1h and 3h Flow cy‐tometry （FCM ） were performed to examine the apoptosis of PBMCs .the secretion of IL‐8 in the culture supernatant of treatment group and control group was tested by ELISA after treated with T‐614 for 24h .Results：We found that iguratimod effectively induced apoptosis in PBMCs .The apoptosis rates of PBMCs treated with T‐614 for 1h were T‐614 8 .23 ± 2 .29% for 50 μg/ml and 12 .30 ± 2 .54% for 500 μg/ml .The apoptosis rates of PBMCs treated with T‐614 for 3h were 13 .39 ± 3 .80% for 50μg/ml and 25 .30 ± 4 .19% for 500μg/ml .Levels of IL‐8 in the culture super‐natant of T‐614 treated group and control group were tested by ELISA .Iguratimod effectively inhibit IL‐8 prodcu‐tion ,48 .91 ± 8 .33 μg/ml for T‐614 50 μg/ml ,125 .31 ± 20 .02μg/ml for T‐614 5μg/ml and 155 .36 ± 22 .15 μg/ml for the control group （treated without T‐614） .Conclusions ：The results suggest that T‐614 induced the apoptosis of PBMCs and inhibited the secretion of IL‐8 in peripheral blood .It might be the possible mechanism of the effect of T‐614 in treatment of RA .
出处
《陕西医学杂志》
CAS
2015年第7期791-793,共3页
Shaanxi Medical Journal
基金
陕西省卫生厅科研资助项目(2012D25)
甘肃省科技厅资助项目(144FKCA060)
