急性肺损伤大鼠吸入一氧化氮后炎症介质变化  

Effect of nitric oxide to acute lung injury mice and the changes of inflammatory factors and endothelial progenitor cells(EPCs)

作　　者：杨智[1] 张靖轩[1] 李燕玲[1] 刘宗师[1] 杨自力[1] 

机构地区：[1]广州医科大学附属广州市第一人民医院重症医学科,广州510180

出　　处：《广州医药》2015年第2期4-7,共4页Guangzhou Medical Journal

基　　金：广州市科技攻关项目(201300000196)

摘　　要：目的观察并评估内毒素性急性肺损伤大鼠吸入一氧化氮后外周血中内皮祖细胞和炎症介质的变化情况。方法 90只SPF级健康大鼠分为3组,A组为正常对照组(n=30),B组为急性肺损伤组(ALI)(n=30),C组为一氧化氮(NO)组(n=30)。分别计算各组外周血内皮祖细胞(Endothelial progenitor cells,EPCs)数量,同时监测肺组织中白细胞介素-10(Interleukin-10,IL-10)水平和髓过氧化物酶(Myeloperoxidase,MPO)活性。结果我们成功建立了大鼠的ALI肺损伤模型,C组EPCs数量、MPO活性上升幅度均小于B组、而IL-10上升水平均高于B组,差异有统计学意义(P<0.05)。结论大鼠吸入一氧化氮可减轻内毒素所致急性肺损伤程度,其机制可能与外周血中内皮祖细胞数量及MPO水平下降和IL-10水平上升有关。Objective To investigate the effect of nitric oxide （NO） inhalation in endotoxin-induced acute lung injury mice. Methods Ninety SPF mice were randomly assigned to the normal group （group A）, ALI group （group B） and ALl ＋ NO group （ group C） . The number of endothelial progenitor cells was counted and the level of Interleukin -10 （IL-10） and my- eloperoxidase （MPO） were measured. Results Endotoxin administration resulted in pulmonary edema. The pulmon edema was lightened and the level of MPO were decreased by the inhalation of nitric oxide while the level of IL-10 increased. Conclu- sion NO inhalation can mitigate acute lung injure. The decline of EPCs and MPO and the increase of IL-10 may be one of the mechanism.

关 键 词：一氧化氮 急性肺损伤 内皮祖细胞髓过氧化酶 白细胞介素-10(IL-10) 

分 类 号：R563.8[医药卫生—呼吸系统]