| Aim: To confirm the anti-inflammation effects of cobrotoxin(CTX) in different inflammatory models and study its anti-arthritic activities in Adjuvant-induced arthritis(AA) rats.Methods: Three tests were used to verify the anti-inflammation effects of CTX. They are formaldehyde-causing mouse foot swelling test, mouse abdominal capillary osmosis test and Whatman paper-inducing rat granuloma formation test. AA rats were as the model of rheumatoid arthritis. The anti-arthritic effects of CTX were evaluated through the arthritis score, paw edema and histopathology changes of joints. The immune level was valued by the proliferation of T cells and the level of CD4 and CD8. The anti-inflammation effects were assayed by the level of IL-6, TNF-α, IL-1β, and the number of inflammatory cells in peripheral blood, as well as the proliferation of fibroblast-like synoviocytes(FLS). The activation of NF-κB was also observed.Results: CTX showed the anti-inflammation effects on different inflammatory models, especially in Whatman paper-inducing rat granuloma formation test. CTX alleviated the disease development of AA rats according to the ameliorating arthritis score, paw edema and histopathology character. At the meanwhile, CTX decreased the levels of IL-6, TNF-α, IL-1β and the numbers of inflammatory cells in peripheral blood. CTX also suppressed the abnormal increasing of CD4+ T cells/ CD8+ T cells ratio, and could significantly inhibit T cell proliferation. Consistent with its effects on inhibiting granuloma’s formation, CTX inhibited the proliferation of the cultured FLSs. Further studies on inflammatory signaling in FLSs revealed that CTX could inhibit the nuclear localization of NF-κB.Conclusions: Our results suggested that CTX exerts anti-inflammation effects in different inflammatory models, and CTX has beneficial effects on AA rats by its immune regulation effects and anti-inflammation effects. NF-κB pathway involves in the anti-inflammatory properties of CTX. |
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