摘要
目的 通过检测肺组织中蛋白激酶B（Akt）、核糖体蛋白S6激酶（p70S6K）水平,探讨后处理措施对肺缺血-再灌注损伤的保护机制.方法 健康雄性SD大鼠24只,数字表法随机分成假手术组（S组）、缺血-再灌注组（I/R组）、缺血后处理组（IpostC组）,每组8只.S组只游离肺门不阻断,2h后取标本;I/R和IpostC组均建立缺血再灌注模型,IpostC组缺血30 min后给予重复5次的30 s灌注和30 s缺血后处理,继而恢复血供行再灌注2h.3组均留取左侧肺组织,应用Western blotting方法测定Akt、磷酸化蛋白少许酶B（p-Akt）、p70S6K、磷酸化核糖体蛋白S6激酶（p-p70S6K）含量;留取小块肺组织测定肺湿/干重比（W/D）,Tunel法测定肺组织细胞凋亡.结果 与S组比较,I/R组、IpostC组肺组织中Akt、p-Akt、p70S6K、p-p70S6K的表达量及W/D值均明显升高（P＜0.05）,凋亡指数显著增加.与I/R组比较,IpostC组肺组织中p-Akt、p70S6K、p-p70S6K的表达量显著增加（P＜0.05）,W/D值与凋亡指数均明显下降（P＜0.05）.结论 后处理可明显减轻大鼠肺缺血再灌注损伤,其机制可能与增强PI3K/Akt信号通路有关.
Abstract： Objective To investigate the protective effect of ischemic postconditioning on lung injury in situ during lung ischemic reperfusion.Methods 24 SD rats were randomly divided into 3 groups,sham-operated group（S）,ischemic-reperfusion group（I/R） and ischemic postconditioning group （IpostC）.IpostC was established by several brief reperfusion-ischemia （30 s,5 cycles） before continuous reperfusion.AKT,p-AKT,p70S6K,p-p70S6K protein expression,apoptotic cells were tested by Western blotting and TUNEL,wet to dry weight ratio（W/D） in lung tissue were determined respectively.The lung pathological changes were also observed.Results Compared with S group,expression of Akt、p-Akt、p70S6K、p-p70S6K and the ratio of W/D,apoptotic index in lung tissue all markedly increased in I/R and IpostC group （P 〈 0.05）.Compared with I/R group,expression of Akt、p-Akt、p70S6K、p-p70S6K markedly increased in IpostC group（P 〈0.05）,while the ratio of W/D and apoptotic index significantly reduced （P 〈 0.05）,the pathological injury in IpostC group also reduced significantly.Conclusion IpostC has a protective effect on lung ischemic reperfusion injury via PI3K/Akt pathway.
出处
《中华胸心血管外科杂志》
CSCD
北大核心
2014年第10期628-631,共4页
Chinese Journal of Thoracic and Cardiovascular Surgery
基金
基金项目：福建省创新医学课题（2009-CXB-62）
