Sheng Liu1, Jun Zhang2, Bentong Yu1, Lei Huang1, Bin Dai1, Jichun Liu1, Jian Tang3. 1. Department of Thoracic Surgery, The First Affiliated Hospital of Nanchang University Jiangxi, PR China. 2. Department of Thoracic Surgery, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology Wuhan, PR China. 3. Department of Thoracic Surgery, The First Affiliated Hospital of Nanchang UniversityJiangxi, PR China; Department of Thoracic Surgery, Union Hospital, Tongji Medical College, Huazhong University of Science and TechnologyWuhan, PR China.
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.
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.
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