Abstract:
BACKGROUND:The aim of this study was to explore the role of autophagy in the cold I/R injury following lung transplantation. METHODS:The rat orthotopic lung transplantation model was established to perform the level of autophagy in the cold I/R injury in this study. The pretreatment of inhibitor (3-Methyladenine [3-MA]) and activator (rapamycin [RAPA]) of autophagy were performed to assess the role of autophagy in the cold I/R injury following lung transplantation in rats. RESULTS:After lung transplantation, the autophagy, lung cell apoptosis and lung injury were aggravated and peaked at 6 h following the transplantation. The inhibition of autophagy by 3-MA induced downregulated of autophagy, decreased cell apoptosis. Meanwhile, the lung injury, which was indicated by calculating the peak inspiratory pressure (PIP), pulmonary vein blood gas analysis (PO2) and ratio of wet to dry in lung (W/D), was ameliorated after treatment with 3-MA. The activation of autophagy by RAPA causing the upregulated of autophagy and apoptosis of lung cells, and enhanced the lung injury. CONCLUSION:All the results suggested that the autophagy was involved in the cold I/R injury in lung transplantation model, and played a potential role on the regulation of I/R injury after lung transplantation.
journal_name
Am J Transl Resjournal_title
American journal of translational researchauthors
Liu S,Zhang J,Yu B,Huang L,Dai B,Liu J,Tang Jsubject
Has Abstractpub_date
2016-08-15 00:00:00pages
3593-602issue
8issn
1943-8141journal_volume
8pub_type
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journal_title:American journal of translational research
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journal_title:American journal of translational research
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