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内毒素所致急性肺损伤发病机制的研究进展
引用本文:李超然,王智刚,朱运奎[审校]. 内毒素所致急性肺损伤发病机制的研究进展[J]. 中国科学美容, 2011, 0(10): 47-49
作者姓名:李超然  王智刚  朱运奎[审校]
作者单位:[1]兰州大学第二医院,甘肃兰州730000 [2]兰州军区兰州总医院呼吸内科,甘肃兰州730000 [3]兰州军区兰州总医院心血管内科,甘肃兰州730000
基金项目:全军医药卫生科研基金资助项目(编号:06G029)
摘    要:
急性肺损伤是临床常见的危重症。内毒素是导致急性肺损伤最常见的原因。近年来关于内毒素所致的急性肺损伤发病机制的研究发现:核转录因子κB、IL-8和中性粒细胞在促炎/抗炎反应的失衡中发挥重要作用,组织因子和肺泡上皮细胞在调节促凝/抗凝反应的失衡中发挥重要作用,而氧化应激和炎症反应之间可以相互促进。而且肺泡上皮细胞和PMN凋亡功能的紊乱、肺泡上皮细胞上Na+通道的下调、PMN释放的中性粒细胞弹性蛋白酶等在LPS导致的ALI发展过程中都发挥重要作用。

关 键 词:急性肺损伤  内毒素  发病机制

Progress in Mechanisms Research of Lipopolysaccharide-induced Acute Lung Injury
Affiliation:LI Chaoran1,2 WANG Zhigang1,3 ZHU Yunkui2 1.The Second Hospital Lanzhou University Lanzhou 730000 China;2.Department of Respiration Internal,Lan zhou General Hospital Military District Lanzhou 730000 China;3.Department of Heart and Blood Vessel Internal,Lanzhou General Hospital of Lanzhou Military District,Lanzhou 730000,China
Abstract:
Acute Lung Injury is the common critical disease in hospital.And the lipopolysaccharide is the most common reason to induce ALI.Recent years,about the mechanisms of LPS-induced ALI researchers found tha:tNF-κB,IL-8 and PMN play an important role in the inflammatory reaction;Tissue factor and alveolar epithelial cells are important in regulating the coagulation;Oxidant stress and inflammatory reaction can facilitate each other.And also,the unnormal apoptosis of AEC and PMN,the down regulation of Na0+ channel in AEC and NE secreted by PMN are all important in the development of LPS-induced ALI.
Keywords:Acute Lung Injury  LPS  Mechanisms
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