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Mediators for the aggravation of acute pancreatitis-the role of cytokies and activated neutrophils

急性胰腺炎加重的介质——细胞因子和活化中性粒细胞的作用

基本信息

批准号：
05454356
负责人：
OGAWA Michio
金额：
$ 4.42万
依托单位：
Kumamoto University
依托单位国家：
日本
项目类别：
Grant-in-Aid for General Scientific Research (B)
财政年份：
1993
资助国家：
日本
起止时间：
1993 至 1994
项目状态：
已结题

项目摘要

The present sudy was undertaken to investigate the roles of cytokines and activated neutrophils on the aggravation of cerulein-induced acute pancreatitis in rats. These mediators may induce multiple organ failures.1.In vitro tumot necrosis factor-alpha (TNF-alpha) production in response to lipopolysaccharide (LPS) by peritoneal macrophages taken from cerulein-induced pancretitis rats was signifcantly enhanced compared to that odserved in naive controls.2.Pancreatitis of non-pancreatitis rats were injected intraperitoneally with LPS as a septic challenge.(1) Serum levels of TNF-alpha in pancreatitis rats with LPS were significantly higher than those in non-pancreatitis rats with LPS.(2) In vitro TNF-alpha production by bronchoalveolar macrophages obtained from pancreatitis rats with LPS were significantly enhaced compared to those in non-pancreatitis rats with LPS.(3) Neutrophil accumulation to the lungs was increased in pancreatitis rats with LPS compared to that in non-pancreatitis ra … More ts with LPS.(4) In addition, myeloperoxidase activity in the lung was significantly increased in pancreatitis rats with LPS.(5) Superoxide production of brochoalveolar macrophages determined by in situ nitro blue terazolium (NBT) method was also enhanced in pancreatis rats with LPS.(6) Liver dysfucntinos were predominantly noted in pancreatitis rats with LPS, serologically and histologically.The survival rates during 24 hours in pancreatitis rats with LPS was significantly shorter than those in non-pancreatitis rats with LPS.The administration of protease inhibitors tends to decrease cytokine production and liver dysfunction in pancreatitis rats with LPS.Thus, hypercytokinemia and remote organ failures were encountered in pancreatitis rats when endotoxemia was involved. In cerulein-induced acute pancreatitis, macrophages could be primed and activated to release a large amount of cytokines when LPS was administared as the second attack. As a result, neutrphils accumulated into the remote organs leading to the tissue destruction. The administation of protease inhibitors trends to ameliorate these organ faulires. However, futrther experiments were required. Less

本研究旨在探讨细胞因子和活化中性粒细胞在蛙皮素诱导的大鼠急性胰腺炎加重中的作用。1.蛙皮素诱导的胰腺炎大鼠腹腔巨噬细胞对脂多糖（LPS）反应产生肿瘤坏死因子-α（TNF-α）的能力明显增强。(1)LPS诱导的胰腺炎大鼠血清TNF-α水平显著高于LPS诱导的非胰腺炎大鼠。(2)在体外培养条件下，LPS诱导的胰腺炎大鼠的支气管肺泡巨噬细胞产生TNF-α的能力显著高于LPS诱导的非胰腺炎大鼠。(3)与非胰腺炎大鼠相比，LPS胰腺炎大鼠肺内神经元蓄积增加， ...更多信息与LPS。(4)此外，肺髓过氧化物酶活性显着增加，在胰腺炎大鼠与LPS。(5)用原位硝基蓝四唑（NBT）法测定胰腺炎大鼠支气管肺泡巨噬细胞产生超氧化物歧化酶的能力也增强。(6)LPS胰腺炎大鼠血清学和组织学检查均发现肝脏功能障碍。LPS胰腺炎大鼠24小时存活率明显低于非LPS胰腺炎大鼠。给予蛋白酶抑制剂可减少LPS胰腺炎大鼠细胞因子的产生和肝脏功能障碍。因此，当内毒素血症时，胰腺炎大鼠会出现高细胞因子血症和远端器官衰竭。在蛙皮素诱导的急性胰腺炎模型中，当给予LPS作为第二次攻击时，巨噬细胞可被激活并释放大量细胞因子。结果，嗜中性粒细胞积聚到远端器官中，导致组织破坏。蛋白酶抑制剂的应用有改善这些器官缺陷的趋势。然而，还需要进一步的实验。少