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  • %0 ART
  • %T Suppression of iNOS expression by fucoidan is mediated by regulation of p38 MAPK, JAK/STAT, AP-1 and IRF-1, and depends on up-regulation of scavenger receptor B1 expression in TNF-α- and IFN-γ-stimulated C6 glioma cells
  • %A HANG DO
  • %A SUHKNEUNG PYO
  • %A SOHN Eun-Hwa
  • %G 0955-2863
  • %I Elsevier
  • %C New York, NY, ETATS-UNIS
  • %D 2010
  • %V 21
  • %N 8
  • %P 671-679
  • %P 9
  • %O Anglais
  • %K Cytokine
  • %K Cytokine
  • %K Vertebrata
  • %K Vertebrata
  • %K Enzyme
  • %K Enzyme
  • %K Transferases
  • %K Transferases
  • %K AP1 transcription factor
  • %K Facteur transcription AP1
  • %K Lignée C6
  • %K Mammalia
  • %K Mammalia
  • %K Neuroglia
  • %K Névroglie
  • %K In vitro
  • %K In vitro
  • %K Cell line
  • %K Lignée cellulaire
  • %K Glial cell
  • %K Cellule gliale
  • %K Gamma interferon
  • %K Interféron gamma
  • %K Tumor necrosis factor α
  • %K Facteur nécrose tumorale α
  • %K Biological receptor
  • %K Récepteur biologique
  • %K Mitogen-activated protein kinase
  • %K Mitogen-activated protein kinase
  • %K Regulation(control)
  • %K Régulation
  • %K Gene expression
  • %K Expression génique
  • %K Fucoidan
  • %K iNOS
  • %K p38
  • %K SRB1
  • %K Glia
  • %X In neurodegenerative disorders, activated glial cells overproduce nitric oxide (NO), which causes neurotoxicity. Inducible NO synthase (iNOS) is a potential therapeutic target in neurodegenerative diseases. Here, we examined the action of fucoidan, a high-molecular-weight sulfated polysaccharide, on tumor necrosis factor-α (TNF-α)- and interferon-γ (IFN-γ)-induced NO production in C6 glioma cells. Fucoidan suppressed TNF-α- and IFN-γ-induced NO production and iNOS expression. In addition, fucoidan inhibited TNF-α- and IFN-γ-induced AP-1, IRF-1, JAK/STAT and p38 mitogen-activated protein kinase (MAPK) activation and induced scavenger receptor B1 (SR-B1) expression. Blocking of sR-B1 did not reverse the inhibitory effect of fucoidan on TNF-α- and IFN-γ- stimulated NO production. However, inhibition of sR-B1 expression by siRNA increased iNOS expression and p38 phosphorylation in TNF-α- and IFN-γ-stimulated C6 cells. Overall, p38 MAPK, AP-1, JAK/STAT and IRF-1 play an important role in the inhibitory effect of fucoidan on TNF-α- and IFN-γ-stimulated NO production, and intracellular SR-B1 expression may be related to the inhibition of iNOS expression by fucoidan via regulation of p38 phosphorylation. The present results also suggest that fucoidan could be a potential therapeutic agent for treating inflammatory-related neuronal injury in neurological disorders. 
  • %S The Journal of nutritional biochemistry

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