2014 Volume 26 Issue 1 Pages 47-56
Fucoidan, a natural sulfated polysaccharide found in the extracellular matrix of brown algae, is rich in L-fucose and sulfate. Fucoidan has a variety of biological actions, including anti-oxidative, anti-coagulative, anti-cancer, and anti-inflammatory activity. However, the cellular molecular mechanism underlying the anti-inflammatory effects of fucoidan remains poorly understood. Rheumatoid arthritis (RA) is a chronic inflammatory disease that causes synovitis and progressive joint destruction. Interleukin (IL) -1β, one of the important mediators involved in the pathogenesis of RA, is known to activate various intracellular signaling pathways. Therefore, in the present study we investigated the inhibitory effects of fucoidan on IL-1β-induced inflammation in human synovial (SW982) cells. SW982 cells were pretreated with fucoidan (100µg/mL) for 1h before cotreatment with 5ng/mL IL-1β plus fucoidan for periods ranging from 20min to 24h. Levels of the proinflammatory mediators IL-6, tumor necrosis factor-α, and cyclooxygenase-2 were then determined. We also assayed translocation of nuclear factor (NF) -κB into the nucleus and activation of mitogen-activated protein kinase (MAPK). Significant increases in the production of proinflammatory mediators were observed from 6 to 24h of IL-1β treatment. The translocation of NF-κB into the nucleus peaked after approximately 6h incubation. After 20min incubation, IL-1β activated c-jun N-terminal kinase and p38 MAPK in SW982 cells. This effect was ameliorated by the coincubation of cells with fucoidan. These results suggest that fucoidan exerts its anti-inflammatory effect by regulating the gene expression of proinflammatory mediators by suppressing the activity of transcription factors and MAPK. Thus, fucoidan may have therapeutic potential for the treatment of RA.