title: [The inhibitory effects of extrinsic carbon monoxide-releasing molecules II on inflammatory responses in liver of mice with severe burns].
abstract: OBJECTIVE
  To investigate the inhibitory effects of extrinsic carbon monoxide-releasing molecules II on inflammatory responses in liver of mice with severe burns and its potential mechanisms.
  
  
  METHODS
  Forty-five male C57BL/6 mice were randomly divided into sham (simulation of burn with 37 degrees C warm water), sham + CORM-2 (with 8 mg/kg CORM-2 after the same manipulation as sham group), burn (with 15% TBSA full-thickness burns), burn + CORM-2 (with 8 mg/kg CORM-2 after the same manipulation as burn group), burn + DMSO (with DMSO after the same treatment as burn group) groups,with 9 mice in each group. The serum level of ALT and AST were determined at 24 post-burn hours (PBH), and the level of myeloperoxidase (MPO), nuclear factor (NF) kappaB, intercellular adhesion molecular (ICAM-1), vascular cell adhesion molecular (VCAM-1), as well as adhesion of polymorphonuclear leucocytes to sinusoidal endothelial cells (HSECs) after serum stimulation were detected and assessed at the same time-points.
  
  
  RESULTS
  The level of ALT and AST (398 +/- 34,122 +/- 22 ), the activity of MPO and NF-kappaB, the protein level of ICAM-1 and VCAM-1 in burn group were obviously increased when compared with those in sham group and burn + CORM-2 group (P < 0.05 or P < 0.01). Additionally, the adhesion of PMN on HSEC after stimulation of serum in burn group was enhanced, while it was markedly inhibited after stimulation of serum in burn + CORM-2 group (P < 0.05).
  
  
  CONCLUSIONS
  Extrinsic CORM-2 exhibits the ability to inhibit NF-kappaB activity, reduces the hepatic expression of ICAM-1 and VCAM-1, thereby alleviating sequestration of leukocytes after severe burns, so that hepatic inflammatory response is ameliorated, and liver function is improved.
authors.affiliation: Department of Burns and Plastic Surgery, Affiliated Hospital of Jiangsu University, Zhenjiang 212001, PR China. sunbinwe@hotmail.com
authors.forename: Bing-Wei
authors.initials: BW
authors.lastname: Sun
authors.forename: Xi
authors.initials: X
authors.lastname: Chen
authors.forename: Zhao-Yong
authors.initials: ZY
authors.lastname: Chen
authors.forename: Katada
authors.initials: K
authors.lastname: Kazuhiro
authors.forename: Cepinskas
authors.initials: C
authors.lastname: Gediminas
mesh_terms: D000818:Animals; D002056:Burns / Q000378:metabolism*; D002248:Carbon Monoxide / Q000378:metabolism*; D002448:Cell Adhesion; D004195:Disease Models, Animal; D007249:Inflammation; D018799:Intercellular Adhesion Molecule-1 / Q000378:metabolism; D008099:Liver / Q000187:drug effects* / Q000378:metabolism*; D008297:Male; D051379:Mice; D008810:Mice, Inbred C57BL; D016328:NF-kappa B / Q000378:metabolism; D009504:Neutrophils / Q000378:metabolism; D009942:Organometallic Compounds / Q000494:pharmacology*; D009195:Peroxidase / Q000378:metabolism; D019010:Vascular Cell Adhesion Molecule-1 / Q000378:metabolism
chemical_list: D016328:NF-kappa B; D009942:Organometallic Compounds; D019010:Vascular Cell Adhesion Molecule-1; C447082:tricarbonyldichlororuthenium (II) dimer; D018799:Intercellular Adhesion Molecule-1; D002248:Carbon Monoxide; D009195:Peroxidase