Ginsenoside metabolite compound K attenuates inflammatory responses of adjuvant-induced arthritis rats

To investigate the effects of ginsenoside metabolite compound K (CK) on adjuvant-induced arthritis (AA) rats and the partial mechanisms focused on the function of immunocyte (B cell and macrophage) and effectors' cell (fibroblast-like synoviocyte, FLS).

Animals were divided randomly into nine groups including control, AA, CK (5, 10, 20, 40, 80, and 160 mg/kg, i.g.), and MTX (0.5 mg/kg, i.g.). The effects of CK on AA rats are evaluated by swelling of the paw, histopathology of joint, and inflammatory cytokine production in serum. To further investigate the effects of CK on the function of B cell, peritoneal macrophage, and FLS from AA rats, we examined the proliferation of B cell and FLS by [3H] thymidine incorporation, and the phagocytic function of peritoneal macrophage was measured by neutral red uptake. Cytokines and antibodies in serum and the supernatant from peritoneal macrophage and FLS were measured by ELISA kit.

CK suppressed the severity of AA rats by attenuating the paw swelling and histopathology of joint. CK can inhibit the proliferation of B cell and autoantibody levels, and suppressed the phagocytic function of peritoneal macrophage and secreted pro-inflammatory cytokines TNF-α, IFN-γ, and IL-17 and up-regulated the level of protective cytokines IL-10. CK attenuated the proliferation of FLS, and balanced the ratio of RANKL to OPG in AA rats.

Our results suggest that CK may attenuate the severity of AA rats, partially by influencing the function of immunocyte (B cell and macrophage) and effectors' cells (FLS) in AA.