Dioscin inhibits IL-17+γδT cells to exert an anti-rheumatoid arthritis effect
- VernacularTitle:薯蓣皂苷抑制IL-17+γδT细胞发挥抗类风湿关节炎作用
- Author:
Lin-mei PU
1
;
Hao-hong ZHANG
;
Chao-yu CHU
;
Yuan-yuan NI
;
Zhao WU
;
Qing-yan MO
;
Hong-yun WANG
;
Ying XU
;
Chun-ping WAN
Author Information
- Publication Type:Journal Article
- Keywords: dioscin; rheumatoid arthritis; collagen-induced arthritis; IL-17; γδT cells; Vδ4 cells
- From: Chinese Pharmacological Bulletin 2025;41(11):2082-2088
- CountryChina
- Language:Chinese
- Abstract: Aim To explore the mechanism by which dioscin regulates IL-17+γδT cells in the treatment of arthritis.Methods A collagen-induced arthritis(CIA)model was established in DBA/1 mice using bovine type Ⅱ collagen.The mice were randomly divid-ed into the CIA model group,methotrexate(MTX)positive control group,and dioscin low-dose(Dioscin-L),medium-dose(Dioscin-M),and high-dose(Dios-cin-H)groups.After intervention,the therapeutic effects were evaluated using scoring methods.Joint pathological damage was analyzed by hematoxylin and eosin(HE)staining.The levels of anti-collagen-spe-cific antibodies and the pro-inflammatory cytokine IL-17 were measured by ELISA.The expressions of γδT cells and their subtypes,as well as the secretion level of IL-17,were detected by flow cytometry.Results Dioscin significantly reduced the arthritis severity score in collagen-induced arthritis(CIA)mice,alleviated joint pathological damage,inhibited the production of IL-17 by splenic lymphocytes and the levels of anti-col-lagen-specific antibodies total IgG and IgG3,and de-creased the proportion of γδT cells in the lymph nodes,splenic γδT cells,and the Vδ4+T-cell subset.The level of IL-17 produced by the Vδ4 subtype in the lymph nodes of the intervention groups was lower than that in the model group,but the difference was not sta-tistically significant.Conclusion Dioscin has signifi-cant therapeutic effect on CIA,and its mechanism may be through the inhibition of γδT cells,but it is unlikely to be related to IL-17 derived from γδT cells.
