title: Nuclear factor-kappaB activation on the reactive oxygen species in acute necrotizing pancreatitic rats.
abstract: OBJECTIVE
  To investigate the potential role of nuclear factor kappa-B (NF-kappaB) activation on the reactive oxygen species in rat acute necrotizing pancreatitis (ANP) and to assess the effect of pyrrolidine dithiocarbamate (PDTC, an inhibitor of NF-kappaB).
  
  
  METHODS
  Rat ANP model was established by retrograde injection of 5% sodium taurocholate into biliopancreatic duct. Rats were randomly assigned to three groups (10 rats each): Control group, ANP group and PDTC group. At the 6th h of the model, the changes of the serum amylase, nitric oxide (NO), malondialdehyde (MDA), superoxide dismutase (SOD) and pancreatic morphological damage were observed. The expressions of inducible nitric oxide (iNOS) were observed by SP immunohistochemistry. And the expressions of NF-kappaB p65 subunit mRNA were observed by hybridization in situ.
  
  
  RESULTS
  Serum amylase and NO level decreased significantly in ANP group as compared with PDTC administrated group ((7 170.40+/-1 308.63) U/L vs (4 074.10+/-1 719.78) U/L, P<0.05), ((76.95+/-9.04) micromol/L vs (65.18+/-9.02) micromol/L, P<0.05) respectively. MDA in both ANP and PDTC group rose significantly over that in control group ((9.88+/-1.52) nmol/L, (8.60+/-1.41) nmol/L, vs (6.04+/-1.78) nmol/L, P<0.05), while there was no significant difference between them. SOD levels in both ANP and PDTC group underwent a significant decrease as compared with that in control ((3 214.59+/-297.74) NU/mL, (3 260.62+/-229.44) NU/mL, vs (3 977.80+/-309.09) NU/mL, P<0.05), but there was no significant difference between them. Though they were still higher than those in Control group, pancreas destruction was slighter in PDTC group, iNOS expression and NF-kappaB p65 subunit mRNA expression were lower in PDTC group as compared with ANP group.
  
  
  CONCLUSIONS
  We conclude that correlation among NF-kappaB activation, serum amylase, reactive oxygen species level and tissue damage suggests a key role of NF-kappaB in the pathogenesis of ANP. Inhibition of NF-kappaB activation may reverse the pancreatic damage of rat ANP and the production of reactive oxygen species.
authors: Department of Surgery, The First Affiliated Hospital, China Medical University, Shenyang 110001, Liaoning Province, China. ljcmu@sina.com
authors: Jin
authors: J
authors: Long
authors: Na
authors: N
authors: Song
authors: Xi-Ping
authors: XP
authors: Liu
authors: Ke-Jian
authors: KJ
authors: Guo
authors: Ren-Xuan
authors: RX
authors: Guo
mesh_terms: D000681:Amylases / Q000378:metabolism; D000818:Animals; D008297:Male; D016328:NF-kappa B / Q000235:genetics / Q000378:metabolism*; D009569:Nitric Oxide / Q000378:metabolism; D019001:Nitric Oxide Synthase / Q000378:metabolism; D052247:Nitric Oxide Synthase Type II; D019283:Pancreatitis, Acute Necrotizing / Q000378:metabolism* / Q000473:pathology; D012333:RNA, Messenger / Q000032:analysis; D051381:Rats; D017208:Rats, Wistar; D017382:Reactive Oxygen Species / Q000378:metabolism*; D051996:Transcription Factor RelA
chemical_list: D016328:NF-kappa B; D012333:RNA, Messenger; D017382:Reactive Oxygen Species; D051996:Transcription Factor RelA; D009569:Nitric Oxide; D019001:Nitric Oxide Synthase; D052247:Nitric Oxide Synthase Type II; C496318:Nos2 protein, rat; D000681:Amylases