title: Evaluation of the suppressive actions of glucosamine on the interleukin-1beta-mediated activation of synoviocytes.
abstract: 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.
  
  
  METHODS
  Synoviocytes isolated from human synovial tissues were stimulated with interleukin (IL)-1beta in the presence of 0.01-1 mM glucosamine. IL-8 and prostaglandin (PG) E(2) 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 [(125)I] IL-1beta to its receptors were examined using a primary human synovial cell line (CSABI- 479).
  
  
  RESULTS
  Glucosamine significantly suppressed the IL-1beta-induced IL-8 production as well as its mRNA expression (p < 0.05) at 1 mM. Furthermore, glucosamine (1 mM) inhibited the IL-1beta-induced nitric oxide and PGE(2) production (p < 0.05). Moreover, glucosamine suppressed the IL-1beta-induced phosphorylation of p38 MAPK (p < 0.05 at >0.1 mM) and the IL-1beta-binding to its receptors (p < 0.05 at 1 mM).
  
  
  CONCLUSIONS
  These observations suggest that glucosamine can suppress the IL-1beta-mediated activation of synoviocytes (such as IL-8-, nitric oxide- and PGE(2)-production, and phosphorylation of p38 MAPK), thereby possibly exhibiting antiinflammatory actions in arthritis.
authors.affiliation: Department of Host Defense and Biochemical Research, Juntendo University, School of Medicine, 2-1-1 Hongo, Bunkyo-ku, Tokyo, 113-8421, Japan.
authors.forename: J
authors.initials: J
authors.lastname: Hua
authors.forename: K
authors.initials: K
authors.lastname: Sakamoto
authors.forename: T
authors.initials: T
authors.lastname: Kikukawa
authors.forename: C
authors.initials: C
authors.lastname: Abe
authors.forename: H
authors.initials: H
authors.lastname: Kurosawa
authors.forename: I
authors.initials: I
authors.lastname: Nagaoka
mesh_terms: D000893:Anti-Inflammatory Agents / Q000494:pharmacology*; D001172:Arthritis, Rheumatoid / Q000188:drug therapy* / Q000276:immunology; D002478:Cells, Cultured; D015232:Dinoprostone / Q000096:biosynthesis; D005944:Glucosamine / Q000494:pharmacology*; D006801:Humans; D053583:Interleukin-1beta / Q000037:antagonists & inhibitors*; D016209:Interleukin-8 / Q000096:biosynthesis / Q000235:genetics; D009569:Nitric Oxide / Q000096:biosynthesis; D010766:Phosphorylation; D012333:RNA, Messenger / Q000032:analysis; D013583:Synovial Membrane / Q000166:cytology / Q000187:drug effects*; D048051:p38 Mitogen-Activated Protein Kinases / Q000378:metabolism
chemical_list: D000893:Anti-Inflammatory Agents; D053583:Interleukin-1beta; D016209:Interleukin-8; D012333:RNA, Messenger; D009569:Nitric Oxide; D048051:p38 Mitogen-Activated Protein Kinases; D015232:Dinoprostone; D005944:Glucosamine