基础医学与临床 ›› 2013, Vol. 33 ›› Issue (9): 1146-1149.

• 研究论文 • 上一篇    下一篇

细胞自噬水平在大鼠缺血/再灌注肺组织内变化及其作用

张俊,王家顺,郑志坤,范凯,乔新伟,王建军   

  1. 华中科技大学同济医学院附属协和医院
  • 收稿日期:2012-08-10 修回日期:2012-11-29 出版日期:2013-09-05 发布日期:2013-08-28
  • 通讯作者: 王建军 E-mail:romewangjianjun@hotmail.com
  • 基金资助:
    缺血预处理在大鼠肺缺血再灌注损伤中的作用及机制研究

Changes in autophagy and its role in rat lung following Ischemia/reperfusion injury

  • Received:2012-08-10 Revised:2012-11-29 Online:2013-09-05 Published:2013-08-28

摘要: 目的 探讨大鼠肺缺血再灌注后肺组织内自噬水平的变化和自噬在肺缺血再灌注损伤的作用。方法 大鼠分为假手术组和缺血1h再灌注0、2、6和24h组,免疫印迹法检测自噬标志蛋白LC3-II的表达,电子显微镜观察细胞内自噬体。自噬抑制剂3-甲基腺嘌呤(3-MA)和安慰剂分别预处理假手术组和缺血再灌注2h组大鼠,HE染色和血气分析检测肺组织损伤程度。结果 LC3-II/Actin比值在缺血1h时即有升高,再灌注2~6h达高峰(P<0.01),再灌注24h恢复至接近假手术组水平。主要在I型肺泡上皮细胞和血管内皮细胞内观察到自噬体。3-MA预处理降低肺组织损伤评分,升高血氧分压,减轻肺缺血再灌注损伤(P<0.05)。结果证实,肺缺血及再灌注诱发肺组织呼吸膜细胞自噬激活,3-MA预处理通过抑制自噬改善肺缺血再灌注损伤。结论 细胞自噬可能是肺缺血再灌注病理生理过程中加重损伤的因素。

关键词: 关键词:肺移植, 缺血再灌注损伤, 自噬, 3-甲基腺嘌呤

Abstract: Objective To explore the level and the role of autophagy in lung ischemia-reperfusion injury. Method Animals were subjected sham operation or ischemia-reperfusion. We detected the LC-3 protein in lung tissue by western blot and observed autophagosomes by electronic microscope. To explored the role of autophagy in lung I/R injury, 3-methyladenine (3-MA) were used to pretreat the Animals. HE stain and blood analysis were used to evaluated lung injury. Result The results indicated that the autophagic flux was elevated during ischemia period, and was significantly enhanced during reperfusion. Inhibition of autophagy by 3-methyladenine (3-MA) ameliorated lung I/R injury, as indicated by index number of lung injury and blood analysis. Conclusion The results demonstrated autophagy might be a scathing factor in lung I/R injury.

Key words: Key words: lung transplantation, ischemia-reperfusion injury, autophagy, 3-MA

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