title: [Effects of p38 mitogen-activated protein kinase in protection of carbon monoxide against lipopolysaccharide induced rat small intestine injury].
abstract: OBJECTIVE
  To investigate the effects of low concentration carbon monoxide (CO) inhalation or intraperitoneal infusion on lipopolysaccharide (LPS) induced rat small intestine injury and to detect the roles of p38 mitogen-activated protein kinase (MAPK) pathway during CO administration.
  
  
  METHODS
  SD rats with small intestine injury induced by 5 mg/kg LPS intravenous injection were challenged by room air, 2.5 x 10(-4)(V/V) CO inhalation or intraperitoneal infusion for 1 h, 3 h and 6 h differently. Then all animals were sacrificed, and the ileum tissues were homogenized for determination the levels of platelet activator factor(PAF) and intercellular adhesion molecule-1 (ICAM-1) with enzyme-lined immunosorbent assay, the pathology with light microscope, and the phosphorylated p38 MAPK expression with Western blot.
  
  
  RESULTS
  Compared with either control, CO inhalation or intraperitoneal infusion group at the same time point, the levels of PAF, ICAM-1 and the phosphorylated p38 MAPK of LPS group were increased (all P < 0.01), but there were no statistics differences at the different time point of this group. PAF and ICAM-1 in both LPS injection + CO inhalation group and LPS injection + CO intraperitoneal infusion group were significantly lower than the corresponding value in LPS injection group at the same time point (all P < 0.05), while the expression of phosphorylated p38 MAPK was further up-regulated than that of LPS injection group (P < 0.05). However, there were no significant differences in these parameters between LPS injection+ CO inhalation group and LPS injection+ CO intraperitoneal infusion group.
  
  
  CONCLUSIONS
  Low concentration CO inhalation and intraperitoneal infusion exerts the similar protection against LPS induced rat small intestine injury via down-regulating PAF and ICAM-1 expression. This may involve the p38 MAPK pathway.
authors.affiliation: Intensive Care Unit, the First Alffiliated Hospital of Nanjing Medical University, Nanjing 210029, China.
authors.forename: Shao-hua
authors.initials: SH
authors.lastname: Liu
authors.forename: Ke
authors.initials: K
authors.lastname: Ma
authors.forename: Bing
authors.initials: B
authors.lastname: Xu
authors.forename: Xin-rong
authors.initials: XR
authors.lastname: Xu
mesh_terms: D000818:Animals; D002248:Carbon Monoxide / Q000494:pharmacology*; D015536:Down-Regulation; D007249:Inflammation / Q000139:chemically induced; D018799:Intercellular Adhesion Molecule-1 / Q000378:metabolism; D007421:Intestine, Small / Q000378:metabolism / Q000473:pathology*; D008070:Lipopolysaccharides / Q000037:antagonists & inhibitors* / Q000633:toxicity*; D008297:Male; D010766:Phosphorylation; D010972:Platelet Activating Factor / Q000378:metabolism; D051381:Rats; D017207:Rats, Sprague-Dawley; D048051:p38 Mitogen-Activated Protein Kinases / Q000378:metabolism*
chemical_list: D008070:Lipopolysaccharides; D010972:Platelet Activating Factor; D018799:Intercellular Adhesion Molecule-1; D002248:Carbon Monoxide; D048051:p38 Mitogen-Activated Protein Kinases