Stigmasterol protects rats from collagen induced arthritis by inhibiting proinflammatory cytokines.

Rheumatoid arthritis (RA) is an autoimmune disorder, in which imbalance in synthesis and production of inflammatory cytokines promotes cartilage and bone destruction. Out of the numerous factors contributing to RA prognosis, the transcription factor NF-kBp65 and p38 mitogen-activated protein kinase (p38MAPK) signaling module has been well implicated as a key regulator of inflammation and downstream signaling events in RA. Stigmasterol (STG) is a natural plant based product exhibiting anti-inflammatory activity, however, the mechanism through which it exhibits anti-inflammatory activity has not been completely understood. The current study aimed to understand the mechanisms underlying the anti-inflammatory effect of STG in the treatment of RA in collagen-induced arthritic (CIA) model of arthritis. Our results showed that STG improved the clinical severity in CIA rats compared to control. The therapeutic effects were related with reduced joint destruction and improved histological alterations. Furthermore, treatment of STG also significantly suppresses the expression of proinflammatory mediators (TNF-α, IL-6, IL-1β, iNOS and COX-2) and increases the expression of anti-inflammatory cytokine (IL-10) through down-regulating the expression of NF-kBp65 (inhibiting p-IKB-α activation) and p38MAPK in joints. In agreement with our results, we can suggest that high therapeutic efficacy of STG against CIA induced inflammation in rats are attributed through the suppressing proinflammatory cytokines.
Competing Interests: Declaration of Competing Interest The authors declare no conflict of interest.
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