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中的作用。方法大鼠分为假手术组和缺血1 h再灌注0、2、6和24 h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2 h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1 h时即有升高,再灌注2～6 h达高峰(P<0.01),再灌注24 h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。
Objective To explore the level and the role of autophagy in lung ischemia-reperfusion injury. Methods 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） was used to pretreat the Animals. HE stain and blood analysis were used to evaluated lung injury. Results 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. Conclusions Autophagy might be a scathing factor in lung I/R injury.
出处
《基础医学与临床》
CSCD
北大核心
2013年第9期1146-1149,共4页
Basic and Clinical Medicine
基金
湖北省自然科学基金(0207040605)
