Rheumatoid arthritis (RA) is growing autoimmune and inflammatory disease that occur due to self-destruction of immune response inducing joint deformity and bone erosion. During the arthritis inducing the swelling, pain… Click to show full abstract
Rheumatoid arthritis (RA) is growing autoimmune and inflammatory disease that occur due to self-destruction of immune response inducing joint deformity and bone erosion. During the arthritis inducing the swelling, pain and inflammation in around the joint and other body organs due to injury of tendons and ligaments. Specneuzhenide (SZ) already proved antioxidant and anti-inflammatory effect against the various diseases. In this experimental study, we scrutinized the anti-arthritic effect of SZ against the complete freund adjuvant (CFA) induced arthritic in rats. Subcutaneously injection of CFA was injected into the subplantar region of the left hind paw for induction the arthritis and rats were divided into different groups and rats received the oral administration of SZ (5, 10 and 15 mg/kg) for 28 days. The body weight, paw swelling arthritic score mRNA expression and biochemical parameters were determined at regular time interval. CFA induced arthritic rats treated with SZ significantly (p < 0.001) enhanced the body weight and decreased the paw swelling, arthritic index and organ (spleen and thymus) index, respectively. SZ treated rats significantly (p < 0.001) decreased the hepatic parameter such as SGPT, SGOT and ALP, anti-CII IgG levels (IgG1 and IgG2A) and inflammatory parameters (COX-2 and PGE2). SZ treated rats significantly (p < 0.001) suppressed the level of MDA and increased the level of GSH, SOD and CAT. SZ treated rats suppressed the inflammatory cytokines such as TNF-α, Il-1β, IL-2, IL-6, IL-16, IL-17 and increased the level of IL-10, TGF-β. SZ treated rats significantly (p < 0.001) suppressed the mRNA expression of Nrf2, HO-1 and NF-κB. On the basis of result, we can say that specneuzhenide protective effect against CFA induced arthritis in rats via alteration of HO-1/Nrf-2 pathway.
               
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