title: Carbon liberated from CO-releasing molecules attenuates leukocyte infiltration in the small intestine of thermally injured mice.
abstract: OBJECTIVE
  To determine whether Carbon (CO) liberated from CO-releasing molecules attenuates leukocyte infiltration in the small intestine of thermally injured mice.
  
  
  METHODS
  Thirty-six mice were assigned to four groups. Mice in the sham group (n = 9) were underwent to sham thermal injury; mice in the burn group (n = 9) received 15% total body surface area full-thickness thermal injury; mice in the burn + CORM-2 group (n = 9) were underwent to the same thermal injury with immediate administration of tricarbonyldichlororuthenium (II) dimer CORM-2 (8 mg/kg, i.v.); and mice in the burn+DMSO group (n = 9) were underwent to the same thermal injury with immediate administration of 160 muL bolus injection of 0.5% DMSO/saline. Histological alterations and granulocyte infiltration of the small intestine were assessed. Polymorphonuclear neutrophil (PMN) accumulation (myeloperoxidase assay) was assessed in mice mid-ileum. Activation of nuclear factor (NF)-kappa B, expression levels of intercellular adhesion molecule-1 (ICAM-1) and inducible heme oxygenase in mid-ileum were assessed.
  
  
  RESULTS
  Treatment of thermally injured mice with CORM-2 attenuated PMN accumulation and prevented activation of NF-kappa B in the small intestine. This was accompanied by a decrease in the expression of ICAM-1. In parallel, burn-induced granulocyte infiltration in mid-ileum was markedly decreased in the burn mice treated with CORM-2.
  
  
  CONCLUSIONS
  CORM-released CO attenuates leukocyte infiltration in the small intestine of thermally injured mice by interfering with NF-kappa B activation and protein expression of ICAM-1, and therefore suppressing the pro-adhesive phenotype of endothelial cells.
authors: Department of Burns and Plastic Surgery, Affiliated Hospital, Jiangsu University, 438 Jiefang Rd, Zhenjiang 212001, Jiangsu Province, China. sunbinwe@hotmail.com
authors: Bing-Wei
authors: BW
authors: Sun
authors: Qin
authors: Q
authors: Jin
authors: Yan
authors: Y
authors: Sun
authors: Zhi-Wei
authors: ZW
authors: Sun
authors: Xi
authors: X
authors: Chen
authors: Zhao-Yong
authors: ZY
authors: Chen
authors: Gediminas
authors: G
authors: Cepinskas
mesh_terms: D000818:Animals; D002056:Burns / Q000378:metabolism; D002244:Carbon / Q000378:metabolism*; D002248:Carbon Monoxide / Q000378:metabolism*; D002465:Cell Movement / Q000187:drug effects; D018882:Heat Stress Disorders / Q000378:metabolism*; D006419:Heme Oxygenase (Decyclizing) / Q000378:metabolism; D007082:Ileum / Q000378:metabolism* / Q000473:pathology*; D018799:Intercellular Adhesion Molecule-1 / Q000378:metabolism; D007421:Intestine, Small / Q000378:metabolism*; D008297:Male; D051379:Mice; D008810:Mice, Inbred C57BL; D016328:NF-kappa B / Q000378:metabolism; D009504:Neutrophils / Q000187:drug effects / Q000473:pathology*; D009942:Organometallic Compounds / Q000494:pharmacology; D009195:Peroxidase / Q000378:metabolism
chemical_list: D016328:NF-kappa B; D009942:Organometallic Compounds; C447082:tricarbonyldichlororuthenium (II) dimer; D018799:Intercellular Adhesion Molecule-1; D002244:Carbon; D002248:Carbon Monoxide; D009195:Peroxidase; D006419:Heme Oxygenase (Decyclizing)