Reumatoid arthritis (RA) is an autoimmune disease which has been studied experimentally using a wide variety of animal models including collagen-induced arthritis (CIA). Using this CIA model we studied the therapeutic effects and mechanism of action of Ebosin, a novel exopolysaccharide produced by Streptomyces sp. 139, on arthritis. Ebosin at 200, 400 and 600 mg/kg/day was orally administered to rats respectively between day 10 and 30 after immunization with chicken type II collagen. With the treatment arthritic progression was remarkably suppressed. Levels of anti-type II collagen-specific antibody, IL-IJJ and TNF-a were significantly lower in the Ebosin-treated CIA rats compared with the untreated controls. In cultured fibroblast-like synoviocytes (FLS), remarkable suppression of IL-1P, TNF-a and IL-6 production was detected at both protein and mRNA levels after Ebosin administration. Ebosin also resulted in lower activities of IL-lp-converting enzyme and TNF-a-converting enzyme in FLS. Based on these results, it is concluded that development and progression of rat CIA can be significantly suppressed by orally-administrated Ebosin. The therapeutic effect may be attributed to its inhibition in the production oflL-1P, TNF-a and IL-6 in the CIA rats.Reumatoid arthritis (RA) is an autoimmune disease which is characterized by persistent synovitis, systemic inflammation and autoantibodies. The synovial membrane is infiltrated by immune cells like macrophages and T cells, resulting in chronic production ofpro-inflammatory cytokines and matrix metalloproteinases (MMPs), leading to cartilage and bone degradation. The pro-inflammatory cytokines such as interleukin-l P (IL-l P), interleukin-6 (IL-6) and tumor necrosis factor-a (TNF-a) produced by innate immune cells play essential roles in pathogenesis of inflammatory arthritis (1-3). In the rat CIA, fibroblast-like synoviocytes (FLS) actively participate in the chronic inflammatory responses as a major cell population in the invasive pannus (4). FLS in the hyperplastic synovital lining layer express high levels of MMPs and angiogenic factors in response to several cytokines including IL-l Pand

Introduction: Osteoarthritis (OA) is a common chronic joint disease characterized by articular cartilage degeneration. OA usually manifests as joint pain, limited mobility, and joint effusion. Currently, the primary OA treatment is non-steroidal anti-inflammatory drugs (NSAIDs). Although they can alleviate the disease's clinical symptoms and signs, the drugs have some side effects. Selenium nanoparticles (SeNPs) may be an alternative to relieve OA symptoms. Materials and Results:We confirmed the anti-inflammatory effect of selenium nanoparticles (SeNPs) in vitro and in vivo experiments for OA disease in this study. In vitro experiments, we found that SeNPs could significantly reduce the expression of nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2), the major inflammatory factors, and had significant anti-inflammatory and anti-arthritic effects. SeNPs can inhibit reactive oxygen species (ROS) production and increased glutathione peroxidase (GPx) activity in interleukin-1beta (IL-1β)-stimulated cells. Additionally, SeNPs down-regulated matrix metalloproteinase-13 (MMP-13) and thrombospondin motifs 5 (ADAMTS-5) expressions, while up-regulated type II collagen (COL-2) and aggrecan (ACAN) expressions stimulated by IL-1β. The findings also indicated that SeNPs may exert their effects through suppressing the NF-κB p65 and p38/MAPK pathways. In vivo experiments, the prevention of OA development brought on by SeNPs was demonstrated using a DMM model. Discussion: Our results suggest that SeNPs may be a potential anti-inflammatory agent for treating OA.