Curcumin is a natural herbal product that has been popularly used to treat
autoimmune diseases in China; however, its effects on
rheumatoid arthritis and its mechanism are not clear. The main purposes of this study are to explore the
therapeutic effects of
curcumin on
collagen-induced arthritis (CIA) rats and the pharmacological mechanism. In the present study, CIA rats were established by injecting bovine
type II collagen.
Curcumin and
methotrexate were then orally administered daily, and the swelling degree of the hind limb joints was scored every two days. Histopathological changes were observed by
hematoxylin-
eosin staining. The levels of
cytokines (TNF-α, IL-1β, IL-17 and TGF-β) were detected by radioimmunoassay, while the expression of IκBα and COX-2 was detected by Western blot. In addition, cell viability was detected by
CCK-8 assay, and the effect of
curcumin on macrophage apoptosis was detected by flow cytometry and TUNEL assay. The results indicated that in vivo
curcumin attenuated the degree of joint swelling of rats and the further development of joint histopathology. Moreover, it downregulated the levels of
cytokines. In vitro
curcumin inhibited the degradation of IκBα and reduced the production of COX-2 in LPS-induced inflammatory RAW264.7 cells. Importantly,
curcumin significantly induced macrophage apoptosis. In conclusion, in this study, we have demonstrated that
curcumin exerts
therapeutic effects on
arthritis in CIA rats and has a strong pharmacological activity on reducing the inflammatory response in macrophages. Its mechanism may be related to the inhibition of the NF-κB signaling pathway and the promotion of macrophage apoptosis.