title: Hyperbaric oxygen reduces inflammatory response in acute pancreatitis by inhibiting NF-kappaB activation.
abstract: OBJECTIVE
  The mechanism of hyperbaric oxygen (HBO) therapy for acute pancreatitis has not been fully clarified yet. The main purpose of this study was to investigate the effect of HBO on nuclear factor kappaB (NF-kappaB) activation and the inflammatory response in rats with acute necrotizing pancreatitis (ANP).
  
  
  METHODS
  A total of 120 male Sprague-Dawley rats were randomly divided into 3 groups (40 in each): control, ANP and ANP + HBO. ANP rat models were established by a retrograde injection of 5% sodium taurocholate into the pancreatic duct. HBO treatment was performed at 2.5-fold absolute atmospheric pressure in 90% oxygen for 1, 3, 5, and 7 h. The activation of NF-kappaB and its inhibitor IkappaBalpha in peripheral blood neutrophilic granulocytes was measured by electrophoretic mobility shift assay and Western blot, respectively. The inflammatory cytokines [interleukin (IL)-2, IL-6, tumor necrosis factor-alpha (TNF-alpha), and intercellular adhesion molecule 1] in the blood were measured by enzyme-linked immunosorbent assay.
  
  
  RESULTS
  The blood levels of inflammatory cytokines and NF-kappaB activation were significantly increased in ANP rats compared to control rats, but IkappaBalpha activation was suppressed. The levels of the elevated inflammatory cytokines were positively correlated with the changes in NF-kappaB activation. After HBO treatment, the blood levels of inflammatory cytokines and NF-kappaB activation were significantly decreased in the ANP + HBO group in a time-dependent manner, but IkappaBalpha activation was increased.
  
  
  CONCLUSIONS
  Our findings suggest that acute pancreatitis is associated with the upregulation of cytokines in blood as well as upregulation of NF-kappaB levels and downregulation of IkappaBalpha activation in peripheral blood neutrophilic granulocytes. In contrast, HBO plays a role in acute pancreatitis treatment by normalizing these changes.
authors.affiliation: Department of General Surgery, Xiangya College of Medicine, Central-South University, Changsha, China. yuxiaoyx4@126.com
authors.forename: X
authors.initials: X
authors.lastname: Yu
authors.forename: Y G
authors.initials: YG
authors.lastname: Li
authors.forename: X W
authors.initials: XW
authors.lastname: He
authors.forename: X R
authors.initials: XR
authors.lastname: Li
authors.forename: B N
authors.initials: BN
authors.lastname: Din
authors.forename: Y
authors.initials: Y
authors.lastname: Gan
authors.forename: M
authors.initials: M
authors.lastname: Xu
mesh_terms: D000681:Amylases / Q000652:urine; D000818:Animals; D001201:Ascites / Q000201:enzymology; D015415:Biomarkers / Q000097:blood*; D004789:Enzyme Activation; D006931:Hyperbaric Oxygenation; D020672:I-kappa B Proteins / Q000097:blood; D018799:Intercellular Adhesion Molecule-1 / Q000097:blood; D007376:Interleukin-2 / Q000097:blood; D015850:Interleukin-6 / Q000097:blood; D008297:Male; D000072000:NF-KappaB Inhibitor alpha; D016328:NF-kappa B / Q000097:blood*; D009504:Neutrophils / Q000201:enzymology; D010179:Pancreas / Q000473:pathology; D019283:Pancreatitis, Acute Necrotizing / Q000097:blood / Q000473:pathology / Q000628:therapy*; D011897:Random Allocation; D051381:Rats; D017207:Rats, Sprague-Dawley; D014409:Tumor Necrosis Factor-alpha / Q000097:blood
chemical_list: D015415:Biomarkers; D020672:I-kappa B Proteins; D007376:Interleukin-2; D015850:Interleukin-6; D016328:NF-kappa B; C000606206:Nfkbia protein, rat; D014409:Tumor Necrosis Factor-alpha; D018799:Intercellular Adhesion Molecule-1; D000072000:NF-KappaB Inhibitor alpha; D000681:Amylases