Abstract
The aim of this study was to investigate the possible mechanisms of action of Tripterygium glycosides (TG) in the treatment of ankylosing spondylitis (AS). In total, 20 patients with active AS received treatment with 20 mg TG tablet (TGT) 3 times per day for 6 weeks. In addition, 20 healthy age- and gender-matched individuals were recruited as the control group. The efficacy measures included the Bath AS disease activity index (BASDAI), erythrocyte sedimentation rate (ESR) and C-reactive protein (CRP) levels. The serum interleukin (IL)-17 levels were measured using ELISA. The expression of CD4(+)CD25(+)CD127(low) regulatory T cells (Tregs) in the peripheral blood was evaluated by flow cytometry. A bivariate correlation analysis was used to determine the association of IL-17 levels with BASDAI, ESR, CRP and CD4(+)CD25(+)CD127(low) Tregs in AS patients. Prior to treatment, the BASDAI, ESR and CRP levels in AS patients were found to be elevated compared to those in healthy controls and were significantly reduced following TGT treatment (P<0.05, P<0.05 and P<0.05, respectively). Prior to treatment, the AS patients exhibited significantly higher IL-17 levels compared to those in healthy controls (P<0.05). Following TGT treatment, the IL-17 levels were significantly reduced in AS patients (P<0.01) but were not significantly different in the control subjects (P>0.05). In addition, prior to treatment, the ratio of CD4(+)CD25(+)CD127(low) Tregs in AS patients was significantly lower compared to that in healthy controls (P<0.05) and it was significantly increased following TGT treatment (P<0.05). The correlation analysis between the BASDAI, ESR or CRP levels and IL-17 revealed a positive linear correlation (P<0.001, P<0.001 and P<0.01, respectively), whereas CD4(+)CD25(+)CD127(low) Tregs were found to be negatively correlated with IL-17 (P<0.01). In conclusion, TGT is efficient for the treatment of AS patients and its mechanism of action may be correlated with the upregulation of CD4(+)CD25(+)CD127(low) Tregs and the downregulation of IL-17 in the peripheral blood.