Curculigoside exerts significant anti-arthritic effects in vivo and in vitro via regulation of the JAK/STAT/NF-κB signaling pathway

The present study aimed to investigate the anti-arthritic effects of curculigoside isolated from the rhizome of Curculigo orchioides Gaertn in vivo and in vitro, as well as to determine the potential underlying mechanisms. A rat model of arthritis was induced with type II collagen. Arthritic rats were treated with curculigoside (50 mg/kg) and blood samples were collected to determine serum levels of tumor necrosis factor (TNF)-α, interleukin (IL)-1β, IL-6, IL-10, IL-12 and IL-17A. Furthermore, indices of the thymus and spleen were determined. The anti-proliferative effects of curculigoside were detected with Cell Counting kit-8 assays in rheumatoid arthritis-derived fibroblast-like synoviocyte MH7A cells. In addition, expression levels of Janus kinase (JAK)1, JAK3, signal transducer and activator of transcription (STAT)3, nuclear factor (NF)-κB p65 and its inhibitor (IκB) were determined by western blotting. The results revealed that curculigoside inhibited paw swelling and arthritis scores in type II collagen-induced arthritic (CIA) rats. Additionally, curculigoside decreased serum levels of TNF-α, IL-1β, IL-6, IL-10, IL-12 and IL-17A in CIA rats. Curculigoside also significantly inhibited MH7A cell proliferation in a time and concentration-dependent manner. Furthermore, treatment downregulated the expression of JAK1, JAK3 and STAT3, and upregulated cytosolic nuclear factor (NF)-κB p65 and IκB. In conclusion, the results of the present study indicated that curculigoside exhibited significant anti-arthritic effects in vivo and in vitro, and the molecular mechanism may be associated with the JAK/STAT/NF-κB signaling pathway.