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The role of glial activation on the pathogenesis of septic encephalopathy

胶质细胞活化在脓毒性脑病发病机制中的作用

基本信息

批准号：
14571440
负责人：
MATSUMI Masaki
金额：
$ 2.24万
依托单位：
Okayama University
依托单位国家：
日本
项目类别：
Grant-in-Aid for Scientific Research (C)
财政年份：
2002
资助国家：
日本
起止时间：
2002 至 2003
项目状态：
已结题

来源：
https://kaken.nii.ac.jp/en/grant/KAKENHI-PROJECT-14571440/
关键词：
Sepsis Heme Oxygenase Carbon Monoxide Endotoxin Heme Intestine Oxidative stress Inflammation 敗血症性脳症グリア細胞

项目摘要

Sepsis often leads to a multiple organ dysfunction syndrome (MODS), a leading cause of death in intensive care units. Symptoms of gram-negative bacterial sepsis can be reproduced experimentally by treatment of animals with LPS, a component of the cell wall of Gram-negative bacteria. LPS is responsible for initiating a series of highly complex cascading events leading to multiple organ damage. Reactive oxygen species are also thought to play an important role as an end-effector molecule. We examined the role of HO-1 induction in the intestinal tissue injury in a rat model of septic MODS produced by intraperitoneal injection of LPS. We found that HO-1 was markedly induced following LPS treatment in the mucosal epithelial cells in the Upper intestine such as the duodenum and the jejunum, whereas HO-1 was hardly expressed and not induced by the same treatment in the lower intestine such as the ileum and the colon. In contrast, the intestinal tissue injury acid inflammation was more pronounced in the lower intestine than in the upper intestine. Pretreatment of animals with HO-1 inhibitor augmented mucosal epithelial cell injuries and inflammation in the upper intestine, but not in the lower intestine, suggesting that HO-1 induction and the maintenance of its appropriate activity appear to be critical in the protection of the intestinal epithelial cells from an oxidative injury induced by LPS, or sepsis.

脓毒症通常导致多器官功能障碍综合征（MODS），这是重症监护病房死亡的主要原因。革兰氏阴性细菌脓毒症的症状可以通过用LPS（革兰氏阴性细菌的细胞壁的组分）治疗动物来实验性地再现。LPS负责启动一系列高度复杂的级联事件，导致多器官损伤。活性氧也被认为作为末端效应分子发挥重要作用。我们研究了HO-1诱导在腹腔注射LPS产生的脓毒性MODS大鼠模型中肠组织损伤中的作用。我们发现，HO-1在LPS处理后，在上肠如十二指肠和空肠的粘膜上皮细胞中被显著诱导，而HO-1在下肠如回肠和结肠中几乎不表达，并且不被相同的处理诱导。相反，肠组织损伤酸性炎症在下肠比在上肠更明显。用HO-1抑制剂预处理动物增强了上肠粘膜上皮细胞损伤和炎症，但在下肠中没有，这表明HO-1诱导和维持其适当的活性似乎在保护肠上皮细胞免受LPS诱导的氧化损伤或脓毒症中至关重要。