通痹颗粒通过TRAF3/PTPN22信号通路调控类风湿关节炎大鼠T细胞自噬实验研究

目的:研究通痹颗粒通过TRAF3/PTPN22信号通路调控类风湿关节炎大鼠T细胞自噬.方法:将佐剂性关节炎(AA)模型Wistar大鼠随机分成RA模型组、雷公藤多苷组、通痹颗粒组、3-MA组、联合组.另设正常对照组.治疗组大鼠采用成人剂量的3倍给药,2次/d,连续16 d.正常对照组以等容积的蒸馏水代替.16 d后处死...

Tongbi granule regulates T cell autophagy in rheumatoid arthritis rats through TRAF3/PTPN22 signaling pathway

Objective:Research on Tongbi granule regulates T cell autophagy in rheumatoid arthritis rats through TRAF3/PTPN22 signaling pathway.Methods:The adjuvant arthritis(AA)model wistar rats were randomly divided into RA model group,tripterygium glycosides group,Tongbi granule group,3-MA group,combination group.A blank control group was also set up.Rats in the treatment group were administered 3 times of which given to the adult,twice a day,for 16 consecutive days.The normal control group was replaced by an equal volume of distilled water.Rats in each group were sacrificed 16 days later,and blood samples and tissues were collected as required for related index testing.The detection indicators include foot plantar swelling thickness,arthritis index,determination of serum tumor necrosis factorα(TNF-α),interleukin 1(IL-1),transforming growth factor-β(TGF-β)content,and determination of the content of tumor necrosis TNF-α,IL-1,and TGF-β.Mouse joint tissue tumor necrosis factor receptor-related factor 3(TRAF3),non-receptor protein tyrosine phosphatase 22(PTPN22)protein and autophagy key regulatory protein complex(Beclin1)protein expression were measured.Results:After treatment,each treatment group was compared with the model group,the thickness of the right foot plantar,arthritis index,serum levels of IL-1,TNF-α,TGF-β,and the protein expression of TRAF3,PTPN22 and Beclin1 were significantly improved(P<0.05).There was no significant difference in the above indicators between the tripterygium polyglycosides group,3-MA group and Tongbi granule group(P>0.05).Compared with other treatment groups,the above indicators in the combination group were significantly improved(P<0.05).Conclusion:The mechanism of Tongbi granules in the treatment of RA model rats may include:up-regulating the TRAF3 gene,down-regulating the expression of PTPN22 and Beclin1,thereby inhibiting T cell autophagy,thereby restoring T cell homeostasis and reducing the release of inflammatory cytokines,relieving rat joint swelling and arthritis state,and then playing a role in the treatment of RA.