title: [The effects of lipopolysaccharide and anti-inflammatory drugs on nuclear factor-kappa B in pulmonary intravascular macrophage].
abstract: OBJECTIVE
  To investigate activation of nuclear factor-kappa B(NF-kappa B) in pulmonary intravascular macrophage (PIM) stimulated with lipopolysaccharide (LPS) and effects of anti-inflammatory drugs dexamethasone (DEX) and aspirin (ASA) on the process.
  
  
  METHODS
  PIMs isolated from three healthy pigs were cultured and divided into four groups: Control group; LPS- stimulated group; DEX- or ASA-treated group. The NF-kappa B activity of nuclear protein extract from the PIMs and the concentration of tumor necrosis factor alpha (TNF-alpha) in the supernatant were measured by electrophoretic mobility shift assay (EMSA) and radioimmunoassay (RIA), respectively.
  
  
  RESULTS
  The activity of NF-kappa B significantly increased from 0.5 hr to 4 hr after LPS stimulation (P < 0.01); The level of TNF-alpha in the supernatant elevated markedly from 1 hr to 2 hr after LPS stimulation (P < 0.01); positive correlation was found between the NF-kappa B activity and the TNF-alpha concentration at 1 hr after LPS stimulation (r = 0.991, P < 0.01). Compared with LPS-stimulated group, both NF-kappa B activity and TNF-alpha concentration were significantly lowered in DEX- or ASA-treated groups (P < 0.01).
  
  
  CONCLUSIONS
  LPS might activate NF-kappa B in the PIMs, and induce the increase of transcription and expression of TNF-alpha gene; Both DEX and ASA could inhibit the activation of NF-kappa B and reduce the release of TNF-alpha.
authors.affiliation: Institute of Respiratory Medicine of PLA, Xinqiao Hospital, Third Military Medical University, Chongqing 400037.
authors.forename: E
authors.initials: E
authors.lastname: Cai
authors.forename: Z
authors.initials: Z
authors.lastname: Chen
authors.forename: W
authors.initials: W
authors.lastname: Wu
mesh_terms: D000818:Animals; D000893:Anti-Inflammatory Agents / Q000494:pharmacology*; D000894:Anti-Inflammatory Agents, Non-Steroidal / Q000494:pharmacology*; D001241:Aspirin / Q000494:pharmacology*; D002478:Cells, Cultured; D003470:Culture Media; D003907:Dexamethasone / Q000494:pharmacology*; D024202:Electrophoretic Mobility Shift Assay; D005938:Glucocorticoids / Q000494:pharmacology*; D006801:Humans; D008070:Lipopolysaccharides / Q000494:pharmacology*; D016676:Macrophages, Alveolar / Q000166:cytology / Q000187:drug effects* / Q000378:metabolism; D008934:Mitogens / Q000494:pharmacology*; D016328:NF-kappa B / Q000378:metabolism*; D012680:Sensitivity and Specificity; D013552:Swine; D014409:Tumor Necrosis Factor-alpha / Q000096:biosynthesis
chemical_list: D000893:Anti-Inflammatory Agents; D000894:Anti-Inflammatory Agents, Non-Steroidal; D003470:Culture Media; D005938:Glucocorticoids; D008070:Lipopolysaccharides; D008934:Mitogens; D016328:NF-kappa B; D014409:Tumor Necrosis Factor-alpha; D003907:Dexamethasone; D001241:Aspirin