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不同剂量脂多糖诱导的大鼠急性肺损伤的凋亡机制研究
Apoptotic mechanisms of acute lung injury induced by different doses of lipopolysaccharide in rats

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DOI:
作者:
贾丽洁，陆菡，张富军，薛庆生，罗艳，于布为
JIA Lijie,LU Han,ZHANG Fujun,XUE Qingsheng,LUO Yan
作者单位:
上海交通大学医学院附属瑞金医院麻醉科
Department of Anesthesiology, Ruijin Hospital, Shanghai Jiaotong University School of Medicine
关键词:
细胞凋亡；冬氨酸半胱氨酸蛋白酶-3；凋亡诱导因子； 脂多糖；急性肺损伤
Apoptosis; Caspase-3; AIF; Lipopolysaccharide; Acute lung injury
摘要:
目的 研究不同剂量脂多糖（LPS）诱导的不同程度急性肺损伤（ALI）的细胞凋亡机制。方法 雄性Sprague-Dawley大鼠20只，随机分为4组：生理盐水对照组、5mg/kg LPS组、10mg/kg LPS组和20mg/kg LPS组。处理6小时后处死动物，分别通过苏木素-伊红染色观察肺组织形态学，肺组织湿/干比值评估肺组织水肿，TUNEL染色法检测肺组织细胞凋亡，蛋白质免疫印记法检测肺组织中天冬氨酸半胱氨酸蛋白酶-3（Caspase-3）和凋亡诱导因子（AIF）的表达水平。结果 不同剂量的LPS诱导产生了不同程度的ALI，其严重程度随LPS剂量的增长而增加；LPS诱导肺泡上皮细胞发生凋亡；与对照组相比，5mg/kg LPS诱导的ALI中活化Caspase-3的表达增加，而10mg/kg和20mg/kg LPS诱导的ALI中，活化AIF的表达增加。结论 不同剂量LPS诱导的ALI中，细胞可经由不同的信号分子调控凋亡，这为ALI的抗凋亡治疗提供了潜在的靶点
Objectives Apoptosis is essential for the pathogenesis of acute lung injury (ALI). Levels of endotoxin contribute various severity of ALI and differential adaptive immune response resulting in apoptosis. The aim of this study is to detect apoptotic mediators in ALI induced by different doses of lipopolysaccharide(LPS). Methods Male Sprague-Dawley rats were randomly assigned to one of four groups: a control group, three groups of LPS (5, 10 or 20 mg/kg, respectively). The lungs were harvested six hours after exposure. The lung biopsy stained with hematoxylin-eosin and wet-to-dry weight ratio were investigated. Apoptosis was determined by the TUNEL staining. Expressions of Caspase-3 and apoptosis inducing factor (AIF) were evaluated by western blot. Results Increased doses of LPS induced ascending severity of ALI. And LPS resulted in apoptosis of epithelial cells. Expressions of cleaved Caspase-3 increased in the ALI administrated with 5 mg/kg LPS. Another, expressions of active AIF increased in the ALI models treated with LPS (10 and 20 mg/kg). Conclusions The results indicate that, apoptotic mechanisms of varying severity of ALI challenged by doses of LPS are different, and that either Caspase-3 or AIF is the important mediator involved. This data appears to raise more reasonable molecular targets for anti-apoptotic strategy in ALI therapy.

 

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