期刊
JOURNAL OF SURGICAL RESEARCH
卷 182, 期 2, 页码 E79-E87出版社
ACADEMIC PRESS INC ELSEVIER SCIENCE
DOI: 10.1016/j.jss.2012.11.014
关键词
Lung ischemia-reperfusion injury; Autophagy; Apoptosis; LC3; 3-Methyladenine; Rapamycin; Transplantation
类别
资金
- Technology Department of Hubei Province, China [02.02.040293]
Background: In response to stress, autophagy is activated and may present as a cell survival mechanism or lead to cell death. Although there has been some progress in studying the function of autophagy in the ischemia-reperfusion (I/R) injury of other organs, little is known about the role autophagy plays in lung I/R injury. Methods: A lung I/R injury model in rats was developed to explore the level of autophagy in lung I/R injury. An inhibitor of autophagy (3-methyladenine [3-MA]) was injected before ischemia to study the role autophagy plays in lung I/R injury. Results: The data indicated that the autophagic flux was elevated during the ischemia period, and was enhanced significantly during reperfusion. Inhibition of autophagy by 3-MA ameliorated lung I/R injury, as indicated by a reduced lung wet/dry ratio, myeloperoxidase activity, and malondialdehyde concentrations. 3-MA pretreatment also reduced cleaved caspase-3 and apoptosis in the lung, as indicated by the terminal deoxynucleotidyl transferase dUTP nick end labeling assay. Conclusions: The results demonstrated that autophagy was involved in the lung I/R pathophysiological process, and it may be a scathing factor in lung I/R injury. Crown Copyright (C) 2013 Published by Elsevier Inc. All rights reserved.
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