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首页> 外文期刊>World Journal of Gastroenterology >Nuclear factor-kappaB activation on the reactive oxygen species in acute necrotizing pancreatitic rats.
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Nuclear factor-kappaB activation on the reactive oxygen species in acute necrotizing pancreatitic rats.

机译：急性坏死胰腺大鼠中活性氧的核因子-κB活化。

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AIM: 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 6(th) 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 signifi-cantly 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) mumol/L vs (65.18+/-9.02) mumol/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. CONCLUSION: 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 ratANP and the production of reactive oxygen species.
机译：目的：研究核因子κB（NF-κB）活化对大鼠急性坏死性胰腺炎（ANP）中活性氧的潜在作用，并评估吡咯烷二硫代氨基甲酸酯（PDTC，NF-κB抑制剂）的作用。方法：通过向胆胰管逆行注射5％牛磺胆酸钠，建立大鼠ANP模型。将大鼠随机分为三组（每组10只）：对照组，ANP组和PDTC组。在模型的第6小时，观察到血清淀粉酶，一氧化氮（NO），丙二醛（MDA），超氧化物歧化酶（SOD）和胰腺形态学损伤的变化。 SP免疫组织化学观察诱导型一氧化氮（iNOS）的表达。通过原位杂交观察NF-κBp65亚基mRNA的表达。结果：与PDTC给药组相比，ANP组的血清淀粉酶和NO水平显着降低（（7 170.40 +/- 1 308.63）U / L vs（4 074.10 +/- 1 719.78）U / L，P <0.05 ），（分别为（（76.95 +/- 9.04）mumol / L与（65.18 +/- 9.02）mumol / L，P <0.05）。 ANP和PDTC组的MDA均显着高于对照组（（9.88 +/- 1.52）nmol / L，（8.60 +/- 1.41）nmol / L，vs（6.04 +/- 1.78）nmol / L，P <0.05），而两者之间没有显着差异。与对照组相比，ANP和PDTC组的SOD水平均显着下降（（3 214.59 +/- 297.74）NU / mL，（3 260.62 +/- 229.44）NU / mL，与（3 977.80 +/-） 309.09）NU / mL，P <0.05），但两者之间无显着差异。尽管PDTC组的胰腺破坏较对照组高，但胰腺破坏较小，PDTC组的iNOS表达和NF-κBp65亚基mRNA表达低于ANP组。结论：我们得出结论，NF-κB活化，血清淀粉酶，活性氧水平和组织损伤之间的相关性暗示了NF-κB在ANP发病中的关键作用。抑制NF-κB活化可能逆转ratANP的胰腺损伤和活性氧的产生。

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