title: Potential protective effect of nuclear factor-κB decoy oligodeoxynucleotides on endotoxin-induced liver injury.
abstract: OBJECTIVE
  We sought to study the protective effects of nuclear factor-κB decoy oligodeoxynucleotides (ODNs) on endotoxin-induced liver injury in a rat model.
  
  
  METHODS
  Sixty Sprague-Dawley rats were randomly divided into a control (n=20), a lipopolysaccharide (LPS) (n=20), and an NF-κB decoy ODN group (n=20). Liver and blood serum samples were collected at 24 hours after the operation. NF-κB binding activity was detected by an electrophoretic mobility shift assay, liver histopathology, by light microscopy; and cell apoptosis, by a terminal-deoxynucleotidyl transferase-mediated deoxyuridine triphosphate nick end-labeling assay. The serum of liver enzyme (aspartate transaminase [AST]) levels were measured using an automated biochemical analyzer and tumor necrosis factor (TNF)-α and interleukin (IL)-6 by enzyme-linked immunosorbent assays.
  
  
  RESULTS
  NF-κB was dramatically activated after endotoxin-induced liver injury. Many hepatocytes underwent degeneration and necrosis in the LPS group. The expressions of AST, TNF-α, and IL-6 were significantly increased compared with the control group (P=.0005), However, NF-κB decoy ODNs altered these undesirable changes. On the other hand, IL-6 expression was not significantly decreased by the NF-κB decoy versus the LPS group (P=.0745).
  
  
  CONCLUSIONS
  NF-κB decoy strategy inhibited the binding activity of NF-κB, thus suppressing production of downstream cytokines which play crucial roles in protection from endotoxin-induced injury.
authors.affiliation: Department of General Surgery, Affiliated Hospital of North Sichuan Medical College, Nanchong, Sichuan, China. lijingdong358@126.com
authors.forename: J D
authors.initials: JD
authors.lastname: Li
authors.forename: Y
authors.initials: Y
authors.lastname: Peng
authors.forename: Q
authors.initials: Q
authors.lastname: Li
authors.forename: J W
authors.initials: JW
authors.lastname: Xiao
authors.forename: J P
authors.initials: JP
authors.lastname: Gong
authors.forename: Z J
authors.initials: ZJ
authors.lastname: Liu
mesh_terms: D000818:Animals; D017209:Apoptosis; D001219:Aspartate Aminotransferases / Q000097:blood; D015415:Biomarkers / Q000097:blood; D056486:Chemical and Drug Induced Liver Injury / Q000209:etiology / Q000235:genetics / Q000378:metabolism / Q000473:pathology / Q000517:prevention & control*; D019610:Cytoprotection; D004195:Disease Models, Animal; D024202:Electrophoretic Mobility Shift Assay; D004797:Enzyme-Linked Immunosorbent Assay; D015316:Genetic Therapy / Q000379:methods*; D020287:In Situ Nick-End Labeling; D007274:Injections, Intraperitoneal; D015850:Interleukin-6 / Q000097:blood; D008070:Lipopolysaccharides; D008099:Liver / Q000378:metabolism* / Q000473:pathology; D008297:Male; D016328:NF-kappa B / Q000235:genetics / Q000378:metabolism*; D009336:Necrosis; D009838:Oligodeoxyribonucleotides / Q000008:administration & dosage*; D051381:Rats; D017207:Rats, Sprague-Dawley; D013997:Time Factors; D014409:Tumor Necrosis Factor-alpha / Q000097:blood
chemical_list: D015415:Biomarkers; D015850:Interleukin-6; D008070:Lipopolysaccharides; D016328:NF-kappa B; D009838:Oligodeoxyribonucleotides; D014409:Tumor Necrosis Factor-alpha; C482199:lipopolysaccharide, E coli O55-B5; D001219:Aspartate Aminotransferases