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首页> 外文期刊>American Journal of Physiology >NF-kappa B activation as a pathological mechanism of septic shock and inflammation.
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NF-kappa B activation as a pathological mechanism of septic shock and inflammation.

机译：NF-κB活化是败血性休克和炎症的病理机制。

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摘要

The pathophysiology of sepsis and septic shock involves complex cytokine and inflammatory mediator networks. NF-kappaB activation is a central event leading to the activation of these networks. The role of NF-kappaB in septic pathophysiology and the signal transduction pathways leading to NF-kappaB activation during sepsis have been an area of intensive investigation. NF-kappaB is activated by a variety of pathogens known to cause septic shock syndrome. NF-kappaB activity is markedly increased in every organ studied, both in animal models of septic shock and in human subjects with sepsis. Greater levels of NF-kappaB activity are associated with a higher rate of mortality and worse clinical outcome. NF-kappaB mediates the transcription of exceptional large number of genes, the products of which are known to play important roles in septic pathophysiology. Mice deficient in those NF-kappaB-dependent genes are resistant to the development of septic shock and to septic lethality. More importantly, blockade of NF-kappaB pathway corrects septic abnormalities. Inhibition of NF-kappaB activation restores systemic hypotension, ameliorates septic myocardial dysfunction and vascular derangement, inhibits multiple proinflammatory gene expression, diminishes intravascular coagulation, reduces tissue neutrophil influx, and prevents microvascular endothelial leakage. Inhibition of NF-kappaB activation prevents multiple organ injury and improves survival in rodent models of septic shock. Thus NF-kappaB activation plays a central role in the pathophysiology of septic shock.
机译：败血症和败血性休克的病理生理学涉及复杂的细胞因子和炎性介质网络。 NF-κB激活是导致这些网络激活的重要事件。败血症过程中NF-κB在脓毒症病理生理中的作用和导致NF-κB活化的信号转导途径已成为深入研究的领域。 NF-κB被多种引起病原性休克综合症的病原体激活。在败血性休克的动物模型和患有败血症的人类受试者中，研究的每个器官中的NF-κB活性均显着增加。较高水平的NF-κB活性与较高的死亡率和较差的临床结果相关。 NF-κB介导大量基因的转录，已知其产物在脓毒症病理生理中起重要作用。那些依赖NF-κB依赖性基因的小鼠对败血性休克的发展和败血症的致死性具有抵抗力。更重要的是，阻断NF-κB通路可纠正败血病。抑制NF-κB活化可恢复系统性低血压，改善败血性心肌功能障碍和血管紊乱，抑制多种促炎基因表达，减少血管内凝血，减少组织中性粒细胞流入并防止微血管内皮渗漏。在败血性休克的啮齿动物模型中，抑制NF-κB激活可防止多器官损伤并提高生存率。因此，NF-κB活化在败血性休克的病理生理中起着核心作用。

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