AIM： To investigate the potential role of nuclear factor kappa-B （NF-κB） activation on the reactive oxygen species in rat acute necrotizing pancreatitis （ANP） and to assess the effect of pyrrolidine dithiocarbam...AIM： To investigate the potential role of nuclear factor kappa-B （NF-κB） 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-κB）.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 6^th 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 bhe expressions of NF-κB 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） μmol/L vs （65.18±9.02） μmol/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：hl.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 bhan those in Control group, pancreas destruction was slighter in PDTC group, iNOS expression and NF-κB p65 subunit mRNA expression were lower in PDTC group as compared with ANP group.CONCLUSION： We conclude that correlation among NF-κB activation, serum amylase, reactive oxygen species level and tissue damage suggests a key role of NF-κB in the pathogenesis of ANP. Inhibition of NF-κB activation may reverse the pancreatic damage of rat ANP and the production of reactive oxygen species.展开更多
文摘AIM： To investigate the potential role of nuclear factor kappa-B （NF-κB） 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-κB）.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 6^th 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 bhe expressions of NF-κB 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） μmol/L vs （65.18±9.02） μmol/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：hl.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 bhan those in Control group, pancreas destruction was slighter in PDTC group, iNOS expression and NF-κB p65 subunit mRNA expression were lower in PDTC group as compared with ANP group.CONCLUSION： We conclude that correlation among NF-κB activation, serum amylase, reactive oxygen species level and tissue damage suggests a key role of NF-κB in the pathogenesis of ANP. Inhibition of NF-κB activation may reverse the pancreatic damage of rat ANP and the production of reactive oxygen species.
