【摘要】 目的:探讨内毒素性急性肺损伤(ALI)肺表面活性蛋白A和B(SP-A,SP-B)表达的变化及其机制。方法:用内毒素脂多糖(LPS)制备Wistar大鼠ALI模型,分别采用ELISA、免疫组化和反转录聚合酶链反应(RT-PCR)方法动态观察LPS致伤后不同时间点肺组织TNF-α,SP-A和SP-B蛋白和mRNA表达的变化。结果:肺组织TNF-α蛋白含量和髓过氧化物酶(MPO)活性分别于LPS致大鼠ALI后0.5 h和1 h时显著高于对照组(P<0.01),2 h时达高峰;肺内SP-B阳性Ⅱ型肺泡上皮细胞数量减少,染色变浅,SP-B蛋白表达逐渐减弱,其灰度值于LPS致伤后2 h时显著高于对照组(P<0.01);肺组织SP-A和SP-B mRNA的表达不同程度减弱,2 h时明显弱于对照组(P<0.05),分别于8 h和4 h时达最低水平。结论:LPS致大鼠ALI时肺组织SP-A和SP-B mRNA的表达减弱,SP-B蛋白含量减少,这可能与多形核粒细胞在肺内的聚集和TNF-α水平的增加有关。更多还原

【Abstract】 Objective: Our purpose was to investigate changes of surfactant proteins A (SP-A) and B(SP-B) after endotoxin lipopolysaccharide (LPS) induced acute lung injury (ALI) and their potential mechanisms. Methods:Levels of tumor necrosis factor-α(TNF-α) in lung were measured by using Enzymo-linked irnmunoadsorbent (ELISA). Expressions of SP-A and SP-B in lung were measured by using immunohistochemistry and reverse transcription polymerase chain reaction ( RT-PCR). Results: After treatment with LPS, level of TNF-a in lung and activity of myeloperoxidase ( MPO) significantly increased than those of control group at 0. 5 and 1 hour ( P < 0. 01) . The values reached peak at 2 hours. The number of type II alveolar epithelial cells positive for SP-B markedly declined, and its average gray value increased significantly compared with the control group at 2 hours( P < 0. 01 ). Levels of transcription of SP-A and SP-B mRNA decreased in different ways. At 2 hours after LPS treatment, both decreased significantly( P < 0.05). The transcription of SP-A mRNA reached the lowest point at 8 hours whereas the SP-B at 4 hours. Conclusion; After LPS-induced ALI in rats, levels of transcription of SP-A and SP-B mRNA both greatly decreased and the amount of SP-B in lung also reduced, which maybe related to polymorphonuclear neutrophil recruitment in the lung and lung TNF-a level increased.更多还原