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1683666 
Journal Article 
Evaluation of the suppressive actions of glucosamine on the interleukin-1 beta-mediated activation of synoviocytes 
Hua, J; Sakamoto, K; Kikukawa, T; Abe, C; Kurosawa, H; Nagaoka, I 
2007 
1 
Inflammation Research
ISSN: 1023-3830
EISSN: 1420-908X 
56 
10 
432-438 
18026701 
WOS:000250513500007 
Objective: Recently, we found that administration of glucosamine to adjuvant arthritis, a model for rheumatoid arthritis, suppressed the progression of arthritis in rats. To clarify its anti-inflammatory mechanism, we evaluated the actions of glucosamine on the activation of synoviocytes in vitro.



Materials and methods: Synoviocytes isolated from human synovial tissues were stimulated with interleukin (IL)-1 beta in the presence of 0.01-1 mM glucosamine. IL-8 and prostaglandin (PG) E, were measured by ELISA, and nitric oxide was quantitated by Griess assay. IL-8 mRNA was detected by RT-PCR. Furthermore, the effect of glucosamine on the phosphorylation of p38 mitogen-activated protein kinase (MAPK) and the binding of [I-125] IL-1 beta to its receptors were examined using a primary human synovial cell line (CS-ABI-479).



Results: Glucosamine significantly suppressed the IL-1 beta-induced IL-8 production as well as its mRNA expression (p < 0.05) at 1 mM. Furthermore, glucosamine (1 mM) inhibited the IL-1 beta-induced nitric oxide and PGE(2) production (p < 0.05). Moreover, glucosamine suppressed the IL-1 beta-induced phosphorylation of p38 MAPK (p < 0.05 at >0.1 mM) and the IL-1 beta-binding to its receptors (p < 0.05 at 1 mM).



Conclusions: These observations suggest that glucosamine can suppress the IL-1 beta-mediated activation of synoviocytes (such as IL-8-, nitric oxide- and PGE(2)-production, and phosphorylation of p38 MAPK), thereby possibly exhibiting anti-inflammatory actions in arthritis. 
glucosamine; synoviocyte; rheumatoid arthritis