title: Anti-inflammatory action of sulfated glucosamine on cytokine regulation in LPS-activated PMA-differentiated THP-1 macrophages.
abstract: OBJECTIVE
  The aim of this study was to evaluate the effect of sulfated glucosamine (SGlc) on the regulation of inflammatory cytokines and profiles involved in immunological activities. Changes in the inflammatory profiles of lipopolysaccharide (LPS)-activated phorbol 12-myristate 13-acetate (PMA)-differentiated THP-1 macrophage models were investigated following SGlc treatment.
  
  
  METHODS
  Human THP-1 macrophages were used to evaluate anti-inflammatory profiles. The cytokine secretion levels were measured by enzyme-linked immunosorbent assay (ELISA). Effects of SGlc on the regulation of mRNA and protein levels were determined using RT-PCR and Western blot analysis. The effect of SGlc on the activation of mitogen-activated protein kinases (MAPKs) and NF-κB protein was also determined by Western blot analysis.
  
  
  RESULTS
  Treatment of THP-1 cells with SGlc inhibited the production of pro-inflammatory cytokines such as tumor necrosis factor-α (TNF-α), interleukin (IL)-1β and IL-6. In addition, SGlc suppressed the mRNA and protein expression levels of inflammatory mediators such as inducible nitric oxide synthase, cyclooxygenase-2, TNF-α, IL-1β, IL-6, 5-lipoxygenase and cytoplasmic phospholipase A(2) in LPS-activated THP-1 macrophages. Furthermore, we confirmed that the LPS-activated transcriptions of MAPKs and NF-κB were inhibited by SGlc treatment in PMA-differentiated THP-1 macrophages.
  
  
  CONCLUSIONS
  These results suggest that SGlc can be considered as a potential anti-inflammatory supplement.
authors.affiliation: Department of Chemistry, Pukyong National University, Busan 608-737, Republic of Korea.
authors.forename: Jung-Ae
authors.initials: JA
authors.lastname: Kim
authors.forename: Byul-Nim
authors.initials: BN
authors.lastname: Ahn
authors.forename: Chang-Suk
authors.initials: CS
authors.lastname: Kong
authors.forename: Se-Kwon
authors.initials: SK
authors.lastname: Kim
mesh_terms: D000893:Anti-Inflammatory Agents / Q000494:pharmacology*; D002454:Cell Differentiation; D002460:Cell Line; D002470:Cell Survival / Q000187:drug effects; D051546:Cyclooxygenase 2 / Q000235:genetics; D016207:Cytokines / Q000037:antagonists & inhibitors* / Q000235:genetics / Q000378:metabolism; D015870:Gene Expression / Q000187:drug effects; D005944:Glucosamine / Q000494:pharmacology*; D006801:Humans; D008070:Lipopolysaccharides; D008264:Macrophages / Q000187:drug effects / Q000378:metabolism; D020928:Mitogen-Activated Protein Kinases / Q000235:genetics / Q000378:metabolism*; D016328:NF-kappa B / Q000235:genetics / Q000378:metabolism*; D009569:Nitric Oxide / Q000037:antagonists & inhibitors* / Q000378:metabolism; D052247:Nitric Oxide Synthase Type II / Q000235:genetics; D054467:Phospholipases A2 / Q000235:genetics; D012333:RNA, Messenger / Q000378:metabolism; D020133:Reverse Transcriptase Polymerase Chain Reaction; D015398:Signal Transduction / Q000187:drug effects; D013755:Tetradecanoylphorbol Acetate / Q000494:pharmacology
chemical_list: D000893:Anti-Inflammatory Agents; D016207:Cytokines; D008070:Lipopolysaccharides; D016328:NF-kappa B; D012333:RNA, Messenger; D009569:Nitric Oxide; C496319:NOS2 protein, human; D052247:Nitric Oxide Synthase Type II; D051546:Cyclooxygenase 2; D020928:Mitogen-Activated Protein Kinases; D054467:Phospholipases A2; D005944:Glucosamine; D013755:Tetradecanoylphorbol Acetate