title: Propofol has anti-inflammatory effects on alveolar type II epithelial cells.
abstract: BACKGROUND
  We investigated whether lipopolysaccharide (LPS) induced inflammation in alveolar epithelial type II (ATII) cells is through cluster of differentiation 14 (CD14) and Toll-like receptor 4 (TLR4) and the effect of different dosages of propofol on the inflammation in primary cultured rat ATII cells.
  
  
  METHODS
  Cultured ATII cells were randomly assigned to one of the following five groups: Group C: untreated group (control) cultured in the absence of propofol and LPS; Group LPS: treated with 1 microg/ml LPS; Group P1: treated with 1 microg/ml LPS and 25 microM propofol; Group P2: treated with 1 microg/ml LPS and 50 microM propofol; Group P3: treated with 1 microg/ml LPS and 100 microM propofol. ATII cells in all groups were cultured at 37 degrees C for 3 h. CD14 and TLR4 mRNA was detected using real-time polymerase chain reaction. Western blot was used to detect CD14 and TLR4 protein expression. CD14 and TLR4 expression on the ATII cells was imaged using immunofluorescence. Tumor necrosis factor-alpha (TNF-alpha) production was determined using an ELISA kit.
  
  
  RESULTS
  LPS stimulation resulted in an increased CD14 and TLR4 expression and increased TNF-alpha production in ATII cells. Propofol, at concentrations > or = 50 microM, significantly (P<0.05) and dose-dependently decreased CD14 and TLR4 mRNA expression and protein expression in ATII cells. This was accompanied by a decrease in TNF-alpha production (P<0.05).
  
  
  CONCLUSIONS
  These results suggest that propofol, at clinically relevant concentrations, can reduce inflammatory responses in LPS-induced ATII cells injury through downregulation of CD14 and TLR4 expression.
authors.affiliation: Department of Anesthesiology, Shengjing Hospital of China Medical University, Shenyang 110004, China.
authors.forename: L
authors.initials: L
authors.lastname: Ma
authors.forename: X
authors.initials: X
authors.lastname: Wu
authors.forename: W
authors.initials: W
authors.lastname: Chen
authors.forename: Y
authors.initials: Y
authors.lastname: Fujino
mesh_terms: D000469:Alkaline Phosphatase / Q000378:metabolism; D018686:Anesthetics, Intravenous / Q000494:pharmacology*; D000818:Animals; D000894:Anti-Inflammatory Agents, Non-Steroidal; D015153:Blotting, Western; D002478:Cells, Cultured; D016207:Cytokines / Q000096:biosynthesis; D004305:Dose-Response Relationship, Drug; D004847:Epithelial Cells / Q000187:drug effects / Q000378:metabolism / Q000473:pathology*; D005455:Fluorescent Antibody Technique; D018950:Lipopolysaccharide Receptors / Q000096:biosynthesis; D008070:Lipopolysaccharides / Q000494:pharmacology; D008297:Male; D046529:Microscopy, Electron, Transmission; D015742:Propofol / Q000494:pharmacology*; D011650:Pulmonary Alveoli / Q000378:metabolism / Q000473:pathology*; D051381:Rats; D017208:Rats, Wistar; D020133:Reverse Transcriptase Polymerase Chain Reaction; D051197:Toll-Like Receptor 4 / Q000096:biosynthesis; D014409:Tumor Necrosis Factor-alpha / Q000378:metabolism
chemical_list: D018686:Anesthetics, Intravenous; D000894:Anti-Inflammatory Agents, Non-Steroidal; D016207:Cytokines; D018950:Lipopolysaccharide Receptors; D008070:Lipopolysaccharides; D051197:Toll-Like Receptor 4; D014409:Tumor Necrosis Factor-alpha; D000469:Alkaline Phosphatase; D015742:Propofol