摘要
为了探讨重组人Ⅱ型肿瘤坏死因子受体-抗体融合蛋白(rh TNFR:Fc)对牛Ⅱ型胶原诱导性关节炎(CIA)大鼠T细胞分化的作用。本研究将40只7周龄雌性DA/Slc大鼠随机分为空白对照组、模型对照组、单次治疗组和多次治疗组,每组10只。制备CIA模型,观察rh TNFR:Fc对CIA大鼠右脚踝炎症和组织破坏的影响及后爪关节匀浆中TNF-α、IL-1β和IL-10水平的影响,结合流式细胞和对炎性因子表达的影响分析rh TNFR:Fc对CIA大鼠T细胞分化的作用机制。研究结果表明,rh TNFR:Fc能够减轻CIA大鼠足趾肿胀和炎症,影响T细胞的分化,并能降低组织匀浆中TNF-α和IL-1β水平升高IL-10水平,并影响滑膜组织中多个炎性因子的表达。rh TNFR:Fc对CIA大鼠关节炎具有明显的抗炎作用,其机制可能是通过抑制TNF-α影响T细胞的分化,进而调控多个炎性因子的表达,从而达到治疗关节炎的效果。
To investigate the effect of recombinant human typeⅡtumor necrosis factor receptor-antibody fusion protein(rh TNFR:Fc)on T cell differentiation in bovine typeⅡcollagen-induced arthritis(CIA)rats.Forty 7-week-old female DA/Slc rats were randomly divided into blank control group,model control group,single treatment group and multiple treatment group,with 10 rats in each group.The CIA model was prepared to observe the effect of rh TNFR:Fc on inflammation and tissue destruction of right ankle in CIA rats and the levels of TNF-α,IL-1βand IL-10 in the hind paw joint homogenate,combined with flow cytometry and the effect on the expression of inflammatory factors,the mechanism of rh TNFR:Fc on T cell differentiation in CIA rats was analyzed.rh TNFR:Fc could attenuate swelling and inflammation of the toes in CIA rats,affect the differentiation of T cells,reduce the levels of TNF-α,IL-1βand increase IL-10 level in tissue homogenates,and affect the expression of multiple inflammatory factors in synovial tissue.rh TNFR:Fc has obvious anti-inflammatory effects on arthritis of CIA rats.The mechanism may be to affect the differentiation of T cells by inhibiting TNF-α,thereby regulating the expression of multiple inflammatory factors and achieving the effect of treating arthritis.
作者
张秀英
董汉玉
魏巧凤
崔彦辉
王树军
张红菊
耿芹
李兰兰
杜晴
王晓丽
董砚奉
Zhang Xiuying;Dong Hanyu;Wei Qiaofeng;Cui Yanhui;Wang Shujun;Zhang Hongju;Geng Qin;Li Lanlan;Du Qing;Wang Xiaoli;Dong Yanfeng(Zibo Central Hospital,Zibo,255036;Zhangdian District People's Hospital,Zibo,255025)
出处
《基因组学与应用生物学》
CAS
CSCD
北大核心
2019年第10期4720-4725,共6页
Genomics and Applied Biology
基金
山东省自然科学基金资助项目(ZR2009CM035)资助