title: Regulation of nitric oxide and prostaglandin E2 production by CSAIDS (SB203580) in murine macrophages and bovine chondrocytes stimulated with LPS.
abstract: OBJECTIVE
  To compare two anti-inflammatory drugs: CSAIDS (SB203580) and hydrocortisone on iNOS and COX-2 expression.
  
  
  METHODS
  Murine macrophages and bovine chondrocytes stimulated with LPS and human OA-affected cartilage were used in this study.
  
  
  METHODS
  The macrophages and chondrocytes were preincubated (30 min) with 0.1-1.0 microM CSAIDS or 10 microM of hydrocortisone before stimulating them with 1-100 microg/ml LPS.
  
  
  METHODS
  The end products of iNOS and COX-2: nitric oxide (NO) and PGE2 were estimated by Greiss method and RIA, respectively.
  
  
  RESULTS
  CSAIDS (1 microM) inhibited the production of NO and PGE2 (p< or =0.01) in bovine chondrocytes, but not in murine macrophages (RAW 264.7) (p< or =0.1). In fact, CSAIDS (in murine macrophages) marginally augmented nitrite accumulation (approximately 20%) at 14-24 h of LPS stimulation. Western blot analysis of COX-2 in bovine chondrocytes show decrease in COX-2 expression by hydrocortisone but not CSAIDS, although hydrocortisone and CSAIDS inhibit PGE2 accumulation. Hydrocortisone inhibited both PGE2 and NO production significantly (p< or =0.01) in murine macrophages. Furthermore, hydrocortisone significantly inhibited (p< or =0.01) PGE2 but marginally (p< or =0.05) NO in bovine chondrocytes.
  
  
  CONCLUSIONS
  These experiments demonstrate differential action of CSAIDS and hydrocortisone on NO and PGE2 production in bovine chondrocytes and RAW 264.7 cells.
authors.affiliation: Department of Rheumatology, Hospital for Joint Diseases, New York, NY 10003, USA.
authors.forename: R
authors.initials: R
authors.lastname: Patel
authors.forename: M G
authors.initials: MG
authors.lastname: Attur
authors.forename: M N
authors.initials: MN
authors.lastname: Dave
authors.forename: S
authors.initials: S
authors.lastname: Kumar
authors.forename: J C
authors.initials: JC
authors.lastname: Lee
authors.forename: S B
authors.initials: SB
authors.lastname: Abramson
authors.forename: A R
authors.initials: AR
authors.lastname: Amin
mesh_terms: D000818:Animals; D000893:Anti-Inflammatory Agents / Q000494:pharmacology*; D002417:Cattle; D002460:Cell Line; D019902:Chondrocytes / Q000187:drug effects* / Q000378:metabolism; D051546:Cyclooxygenase 2; D015232:Dinoprostone / Q000096:biosynthesis*; D006801:Humans; D006854:Hydrocortisone / Q000494:pharmacology*; D007093:Imidazoles / Q000494:pharmacology*; D007527:Isoenzymes / Q000096:biosynthesis / Q000187:drug effects; D008070:Lipopolysaccharides / Q000276:immunology; D008264:Macrophages / Q000187:drug effects* / Q000378:metabolism; D008565:Membrane Proteins; D051379:Mice; D009569:Nitric Oxide / Q000378:metabolism*; D011451:Prostaglandin-Endoperoxide Synthases / Q000096:biosynthesis / Q000187:drug effects; D011725:Pyridines / Q000494:pharmacology*
chemical_list: D000893:Anti-Inflammatory Agents; D007093:Imidazoles; D007527:Isoenzymes; D008070:Lipopolysaccharides; D008565:Membrane Proteins; D011725:Pyridines; D009569:Nitric Oxide; D051546:Cyclooxygenase 2; C496540:PTGS2 protein, human; D011451:Prostaglandin-Endoperoxide Synthases; D015232:Dinoprostone; C093642:SB 203580; D006854:Hydrocortisone