过长的冷缺血保存时间激活线粒体氧化应激导致的供肺损伤是降低肺移植供肺利用率的重要原因之一。多个研究表明肠外营养成分L-丙氨酰-L-谷氨酰胺（L-alanyl-L-glutamine）对不同类型肺损伤通过调节氧化应激展现出良好的保护作用，但目前尚缺乏L-alanyl-L-glutamine对供肺冷保存损伤作用的探索。我们的前期研究结果表明，在支气管上皮细胞BEAS-2B及肺血管内皮细胞HPMEC的冷缺血过程中应用L-alanyl-L-glutamine能显著提高冷保存后细胞的活性并抑制细胞凋亡，同时证明体外肺灌注EVLP对评估供肺冷保存改良效果有重要价值。本课题将首次以细胞EVLP和大鼠EVLP模型作为评估供肺冷保存改良效果的新途径，探索冷缺血过程中应用L-丙氨酰-L-谷氨酰胺通过减轻线粒体氧化应激，改善供肺冷保存质量的作用和机制。本课题研究结果将为临床改良供肺冷保存条件提供新的指导。

Prolonged donor lung cold ischemia time induced lung injury by activating mitochondria oxidative stress is one of the most important reasons that leads to the decrease of lung utilization during lung transplantation. An important parenteral nutrition additive L-alanyl-L-glutamine has been demonstrated to have multiple protective effects in different kinds of lung injury through its regulation of mitochondria oxidative stress, but its effects on donor lung cold ischemia injury remain unclear. Our preliminary data showed that cold preservation with L-alanyl-L-glutamine significantly increased the cell viability and decreased the cell apoptosis in both lung epithelial cells BEAS-2B and lung microvascular endothelial cells HPMEC, we also proved that EVLP is of great value in evaluating the effect of donor lung cold preservation. We will further demonstrate the protective effects of L-alanyl-L-glutamine on lung cells and Rat lung during cold ischemia time and explore the potential mechanism of L-alanyl-L-glutamine regulating mitochondria oxidative stress by use the EVLP cell culture model and EVLP Rat model as new evaluating platforms. These findings in our study will contribute as pre-clinical data and provide new hints to modify the lung cold preservation condition in clinical.