摘要
目的探讨胶原诱导的大鼠类风湿性关节炎(RA)模型中,Th22和白细胞介素-22(IL-22)的水平及其可能的机制。方法构建胶原诱导的大鼠RA模型后,流式细胞术检测Th22细胞,Real-time PCR检测IL-22 m R N A表达水平,ELISA检测IL-22蛋白表达水平;用IL-22封闭抗体中和R A大鼠体内IL-22后,CCK-8实验检测R AFLS细胞增殖,R eal-time PCR检测IL-22和STAT3 m R N A表达水平,Western blot检测STAT3蛋白表达水平。结果与对照组比较,RA大鼠全血中的Th22细胞和血清IL-22的表达显著增加(P<0.01);用IL-22封闭抗体中和R A大鼠体内IL-22后,与对照组比较,R A大鼠血清IL-22显著下降(P<0.01),R AFLS细胞增殖能力下降(P<0.01),R AFLS细胞中STAT3基因和蛋白水平的表达显著较少(P<0.01)。结论R A大鼠模型中,Th22细胞通过分泌过多的IL-22刺激STAT3信号途径,从而提升R AFLS细胞的增殖能力,参与大鼠RA的发病。
Objective To investigate the percentage of Th22 cells and the serum IL22 level in the rat model of collagen-induced rheumatoid arthritis（RA）,and to study the mechanism of IL22 on RA.Methods After the model of collagen-induced RA was built,Th22 cells were detected by flow cytometry,the m RNA level of IL22 was detected by real-time PCR,and IL22 protein level was detected by ELISA.After the RA rats were injected with IL22 blocking antibody,the proliferation of rheumatoid arthritis fibroblast-like synoviocytes（RAFLS）was observed by CCK-8,the m RNA levels of IL22 and Stat3 were detected by real-time PCR,the level of STAT3 protein was observed by Western blot.Results The percentage of Th22 cells and the serum IL22 in the peripheral blood of RA rats were significantly higher than those in the control rats（P〈 0.01）.After the RA rats were injected with IL22 blocking antibody,the expression of serum IL22 decreased（P〈 0.01）and the proliferation of RAFLS decreased（P〈 0.01）,the levels of Stat3 m RNA and STAT3 protein also significantly reduced（P〈 0.01）.Conclusions Th22 cells are involved in the pathogenesis of RA in the rat model by stimulating STAT3 signaling pathway through IL22 secretion,which in turn promotes RAFLS proliferation.
出处
《中国现代医学杂志》
CAS
北大核心
2016年第2期1-5,共5页
China Journal of Modern Medicine
