title: [Effect of TNF-alpha monoclonal antibody on tissue lipopolysaccharide-binding protein mRNA expression in rats after thermal injury].
abstract: OBJECTIVE
  To explore the effects of tumor necrosis factor-alpha (TNF-alpha) monoclonal antibody (MAb) on tissue TNF-alpha and lipopolysaccharide-binding protein (LBP) mRNA expression, and multiple organ dysfunction in rats after thermal injury.
  
  
  METHODS
  24 male Wistar rats were subjected to a 35% total body surface area full-thickness thermal injury.
  
  
  RESULTS
  The tissue TNF-alpha and LBP mRNA expressions of liver, lung, intestine, and kidney were markedly increased (P < 0.05 approximately equal 0.01) after thermal injury. Treatment with TNF-alpha MAb could significantly lower TNF-alpha mRNA expression of lung, intestine and kidney, but had no effect on liver TNF-alpha mRNA expression (P > 0.05). Similarly, the tissue LBP mRNA expression also decreased significantly (36.0% - 72.9%), and returned to normal in lung, intestine and kidney. In addition, biochemical parameters including GPT, TBiL, BUN, CK-MB, and LDH were markedly elevated after thermal injury, and decreased significantly after treatment with TNF-alpha MAb.
  
  
  CONCLUSIONS
  The increase of tissue TNF-alpha gene expression caused by thermal injury might be associated with a marked elevation of tissue LBP mRNA expression, which could contribute to the development of multiple organ dysfunction. The early use of TNF-alpha MAb seems to be effective in inhibiting significant LBP mRNA expression in various tissues and ameliorating multiple organ damage after major thermal injury.
authors.affiliation: Trauma Research Center, 304th Hospital of People's Liberation Army, Beijing 100037.
authors.forename: H
authors.initials: H
authors.lastname: Zhai
authors.forename: Y
authors.initials: Y
authors.lastname: Yao
authors.forename: L
authors.initials: L
authors.lastname: Lu
authors.forename: W
authors.initials: W
authors.lastname: Fang
authors.forename: Y
authors.initials: Y
authors.lastname: Yu
authors.forename: Z
authors.initials: Z
authors.lastname: Shi
authors.forename: B
authors.initials: B
authors.lastname: Zhou
authors.forename: H
authors.initials: H
authors.lastname: Tian
authors.forename: Z
authors.initials: Z
authors.lastname: Sheng
mesh_terms: D000209:Acute-Phase Proteins; D000410:Alanine Transaminase / Q000097:blood; D000818:Animals; D000911:Antibodies, Monoclonal / Q000494:pharmacology*; D001663:Bilirubin / Q000097:blood; D001806:Blood Urea Nitrogen; D002056:Burns / Q000235:genetics*; D002352:Carrier Proteins / Q000235:genetics*; D003402:Creatine Kinase / Q000097:blood; D052279:Creatine Kinase, MB Form; D005786:Gene Expression Regulation / Q000187:drug effects; D007413:Intestinal Mucosa / Q000378:metabolism; D007422:Intestines / Q000187:drug effects; D007527:Isoenzymes / Q000097:blood; D007668:Kidney / Q000187:drug effects / Q000378:metabolism; D007770:L-Lactate Dehydrogenase / Q000097:blood; D008099:Liver / Q000187:drug effects / Q000378:metabolism; D008168:Lung / Q000187:drug effects / Q000378:metabolism; D008297:Male; D008562:Membrane Glycoproteins; D012333:RNA, Messenger / Q000187:drug effects* / Q000235:genetics / Q000378:metabolism; D051381:Rats; D017208:Rats, Wistar; D014409:Tumor Necrosis Factor-alpha / Q000235:genetics* / Q000276:immunology; D000099231:Lipopolysaccharide-Binding Protein
chemical_list: D000209:Acute-Phase Proteins; D000410:Alanine Transaminase; D000911:Antibodies, Monoclonal; D001663:Bilirubin; D002352:Carrier Proteins; D003402:Creatine Kinase; D052279:Creatine Kinase, MB Form; D007527:Isoenzymes; D007770:L-Lactate Dehydrogenase; D008562:Membrane Glycoproteins; D012333:RNA, Messenger; D014409:Tumor Necrosis Factor-alpha; D000099231:Lipopolysaccharide-Binding Protein