title: Protection of carbon monoxide inhalation on lipopolysaccharide-induced multiple organ injury in rats.
abstract: OBJECTIVE
  To observe the protection of carbon monoxide (CO) inhalation on lipopolysaccharide (LPS)-induced rat multiple organ injury.
  
  
  METHODS
  Sprague-Dawley rats with multiple organ injury induced by 5 mg/kg LPS intravenous injection were exposed to room air or 2. 5 x 10(-4) (V/V) CO for 3 hours. The lung and intestine tissues of rats were harvested to measure the expression of heme oxygenase-1 (HO-1) with reverse transcription-polymerase chain reaction, the levels of pulmonary tumor necrosis factor-alpha (TNF-alpha), interleukin-6 (IL-6), and intestinal platelet activator factor (PAF), intercellular adhesion molecule-1 (ICAM-1) with enzyme-linked immunosorbent assay, the content of maleic dialdehyde (MDA) and the activity of myeloperoxidase (MPO) with chemical method, the cell apoptosis rate with flow cytometry, and the pathological changes with light microscope.
  
  
  RESULTS
  CO inhalation obviously up-regulated the expression of HO-1 in lung (5.43 +/- 0.92) and intestine (6.29 +/- 1.56) in LPS + CO group compared with (3.08 +/- 0.82) and (3.97 +/- 1.16) in LPS group (both P < 0.05). The levels of TNF-alpha, IL-6 in lung and PAF, ICAM-1 in intestine of LPS + CO group were 0.91 +/- 0.25, 0.64 +/- 0.05, 1.19 +/- 0.52, and 1.83 +/- 0.35 pg/mg, respectively, significantly lower than the corresponding values in LPS group (1.48 +/- 0.23, 1.16 +/- 0.26, 1.84 +/- 0.73, and 3.48 +/- 0.36 pg/mg, all P < 0.05). The levels of MDA, MPO, and cell apoptosis rate in lung and intestine of LPS + CO group were 1.02 +/- 0.23 nmol/mg, 1.74 +/- 0.17 nmol/mg, 7.18 +/- 1.62 U/mg, 6.30 +/- 0.97 U/mg, 1.60% +/- 0.34%, and 30. 56% +/- 6.33%, respectively, significantly lower than the corresponding values in LPS group (1.27 +/- 0.33 nmol/mg, 2.75 +/- 0.39 nmol/mg, 8.16 +/- 1.49 U/mg, 7.72 +/- 1.07 U/mg, 3.18% +/- 0.51%, and 41.52% +/- 3.36%, all P < 0.05). In addition, injury of lung and intestine induced by LPS was attenuated at presence of CO inhalation.
  
  
  CONCLUSIONS
  CO inhalation protects rat lung and intestine from LPS-induced injury via anti-oxidantion, anti-inflammation, anti-apoptosis, and up-regulation of HO-1 expression.
authors.affiliation: Intensive Care Unit, the First Affiliated Hospital of Nanjing Medicial University, Nanjing 210029. liush67@hotmail.com
authors.forename: Shao-hua
authors.initials: SH
authors.lastname: Liu
authors.forename: Xin-rong
authors.initials: XR
authors.lastname: Xu
authors.forename: Ke
authors.initials: K
authors.lastname: Ma
authors.forename: Bing
authors.initials: B
authors.lastname: Xu
mesh_terms: D000818:Animals; D001483:Base Sequence; D002248:Carbon Monoxide / Q000008:administration & dosage*; D017931:DNA Primers; D019570:Inhalation Exposure; D008070:Lipopolysaccharides / Q000633:toxicity*; D008297:Male; D009102:Multiple Organ Failure / Q000139:chemically induced*; D051381:Rats; D017207:Rats, Sprague-Dawley
chemical_list: D017931:DNA Primers; D008070:Lipopolysaccharides; D002248:Carbon Monoxide