Nuclear factor (NF)-kappaB plays a central role in acute pancreatitis. We studied cerulein (CER)-induced pancreatitis in NF-kappaB knockout (KO) mice. NF-kappaB KO mice and normal control littermate wild-type (WT) mice were given four hyperstimulating doses of cerulein every hour to elicit secreatagogue-induced pancreatitis. Malonildialdehyde activity, glutathione levels, myeloperoxidase activity, TNF-alpha, and NF-kappaB binding activity and its inhibitory protein IkappaBalpha were studied in the pancreas. Furthermore, we measured plasma lipase and amylase and the histological damage. KO mice had reduced malonildialdehyde levels (WT + CER = 4.083 +/- 0.95 micromol/g; KO + CER = 1.513 +/- 0.63 microol/g), decreased myeloperoxidase activity (WT + CER = 19.3 +/- 2.39 mU/g; KO + CER = 10.21 +/- 2.05 mU/g), increased glutathione levels (WT + CER 6.22 +/- 2.46 micromol/g; KO + CER = 15. 516 +/- 2.92 micromol/g), and reduced serum levels of amylase (WT + CER = 2519 +/- 656.9 U/L; KO + CER = 916 +/- 280.4 U/L) and lipase (WT + CER = 1420 +/- 170 U/L; KO + CER = 861 +/- 172. 3 U/L). KO mice showed reduced pancreatic NF-kappaB activation, decreased TNF-alpha tissue content, and reduced histologic alterations. Our data suggest that KO mice have an attenuated cerulein-induced pancreatitis and help to define the possible interaction between NF-kappaB activation and oxidative stress in this deleterious event.

中文翻译：

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核因子-kappaB 缺陷小鼠中雨蛙素诱导的胰腺炎减弱。

核因子 (NF)-kappaB 在急性胰腺炎中起着核心作用。我们研究了 NF 活化 (KO) 小鼠中的雨蛙肽 (CER) 诱导的胰腺炎。NF-kappaB KO 小鼠和正常对照同窝野生型 (WT) 小鼠每小时接受四次超刺激剂量的雨蛙素，以引发促分泌素诱导的胰腺炎。在胰腺中研究了丙二醛活性、谷胱甘肽水平、髓过氧化物酶活性、TNF-α 和 NF-kappaB 结合活性及其抑制蛋白 IkappaBalpha。此外，我们还测量了血浆脂肪酶和淀粉酶以及组织学损伤。KO 小鼠丙二醛水平降低（WT + CER = 4.083 +/- 0.95 微摩尔/克；KO + CER = 1.513 +/- 0.63 微摩尔/克），髓过氧化物酶活性降低（WT + CER = 19.3 +/- 2.39 mU/g ; KO + CER = 10.21 +/- 2.05 mU/g)，增加的谷胱甘肽水平 (WT + CER 6. 22 +/- 2.46 微摩尔/克；KO + CER = 15. 516 +/- 2.92 微摩尔/克）和淀粉酶血清水平降低（WT + CER = 2519 +/- 656.9 U/L；KO + CER = 916 +/- 280.4 U/L）和脂肪酶（WT + CER = 1420 +/- 170 U/L；KO + CER = 861 +/- 172. 3 U/L）。KO 小鼠显示胰腺 NF-kappaB 活化减少，TNF-α 组织含量减少，组织学改变减少。我们的数据表明，KO 小鼠的雨蛙素诱导的胰腺炎有所减轻，有助于确定 NF-kappaB 激活与氧化应激在这一有害事件中可能存在的相互作用。减少 TNF-α 组织含量，并减少组织学改变。我们的数据表明，KO 小鼠的雨蛙素诱导的胰腺炎有所减轻，有助于确定 NF-kappaB 激活与氧化应激在这一有害事件中可能存在的相互作用。减少 TNF-α 组织含量，并减少组织学改变。我们的数据表明，KO 小鼠的雨蛙素诱导的胰腺炎有所减轻，有助于确定 NF-kappaB 激活与氧化应激在这一有害事件中可能存在的相互作用。