抑制核因子-κB激活可提高牛磺胆酸盐性胰腺炎大鼠的存活率。
Inhibition of nuclear factor-kappaB activation improves the survival of rats with taurocholate pancreatitis.
作者信息
Satoh A, Shimosegawa T, Fujita M, Kimura K, Masamune A, Koizumi M, Toyota T
机构信息
Third Department of Internal Medicine, Tohoku University School of Medicine, Sendai, Miyagi, Japan.
出版信息
Gut. 1999 Feb;44(2):253-8. doi: 10.1136/gut.44.2.253.
BACKGROUND
Death in the early stages of severe acute pancreatitis is frequently the result of multiple organ dysfunction, but its mechanism is not clear.
AIMS
To investigate the state of nuclear factor-kappaB (NF-kappaB) in macrophages of rats with lethal pancreatitis, and to assess the effectiveness of pyrrolidine dithiocarbamate, an inhibitor of NF-kappaB, on the pathology and mortality.
METHODS
Taurocholate pancreatitis was produced in rats, and the severity of the disease, the mortality, and activation of NF-kappaB in peritoneal and alveolar macrophages were compared in rats receiving pyrrolidine dithiocarbamate (PDTC) treatment and those that were not.
RESULTS
Taurocholate pancreatitis produced massive necrosis, haemorrhage, and severe leucocyte infiltration in the pancreas as well as alveolar septal thickening in the lung. NF-kappaB was activated in peritoneal and alveolar macrophages six hours after pancreatitis induction. Pretreatment with PDTC dose-dependently attenuated the NF-kappaB activation and improved the survival of the rats, although it did not affect the early increase in serum amylase and histological findings.
CONCLUSIONS
Early blockage of NF-kappaB activation may be effective in reducing fatal outcome in severe acute pancreatitis.
背景
重症急性胰腺炎早期死亡常因多器官功能障碍，但机制不明。
目的
研究致死性胰腺炎大鼠巨噬细胞中核因子-κB（NF-κB）的状态，并评估NF-κB抑制剂吡咯烷二硫代氨基甲酸盐对病理学及死亡率的影响。
方法
在大鼠中诱发牛磺胆酸盐胰腺炎，比较接受吡咯烷二硫代氨基甲酸盐（PDTC）治疗的大鼠和未接受治疗的大鼠的疾病严重程度、死亡率以及腹膜和肺泡巨噬细胞中NF-κB的激活情况。
结果
牛磺胆酸盐胰腺炎导致胰腺出现大量坏死、出血和严重白细胞浸润，以及肺部肺泡间隔增厚。胰腺炎诱导后6小时，腹膜和肺泡巨噬细胞中的NF-κB被激活。PDTC预处理可剂量依赖性地减弱NF-κB激活并提高大鼠存活率，尽管它不影响血清淀粉酶早期升高及组织学表现。
结论
早期阻断NF-κB激活可能有效降低重症急性胰腺炎的致命结局。
Zotero 插件