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)