Ⅱ型肺泡上皮细胞（ATⅡ）的损伤和凋亡是脓毒症急性呼吸窘迫综合症（ARDS）发生发展的重要原因，可以定向分化为ATⅡ的骨髓间充质干细胞（BMSC）有望用于ARDS的治疗。我们前期研究证实BMSC和肺内免疫细胞共培养时具有显著的抗凋亡作用，并继而初步建立起诱导高表达Foxm1的BMSC分化为ATⅡ的细胞分化体系，但是，高表达Foxm1的BMSC分化为ATⅡ的详细机制，以及将其应用于治疗脓毒症ARDS的体内外研究，目前罕有报道，由此，本项目拟在前期基础上继续探索Foxm1对BMSC定向分化为ATⅡ的影响及其可能分子机制，同时将靶向上调或下调Foxm1表达的BMSC移植入脓毒症ARDS小鼠模型体内，验证其是否具有改善ARDS肺损伤的生物学作用。本研究旨在探索Foxm1在BMSC高效定向分化为ATⅡ并应用于治疗脓毒症ARDS的潜在重要价值，从而为寻找ARDS新型治疗方法提供理论和实验依据。

Type II alveolar epithelial cells (AT Ⅱ) damage and apoptosis is an important cause of the formation and development in sepsis induced acute respiratory distress syndrome (ARDS), while bone marrow mesenchymal stem cells (BMSC) which can differentiate into AT Ⅱ are expected to be used in the treatment of ARDS. Our previous study has showed that BMSC had an anti-apoptotic effect when co-cultured with lung immune cells，and we has simultaneously established BMSC which highly expressed Foxm1 and differentiated into AT II. However, the detailed mechanism of how the BMSC differentiated into AT II, and its practically application and value in the treatment of septic ARDS in vitro and in vivo studies were rarely reported. Therefore, our project plans to keep investigating the molecular mechanism of how BMSC with differently expression of Foxm1 differentiated into AT II in the preliminary basis, at the same time, we will transplant the stably transfected BMSC into sepsis mouse model of ARDS in vivo, in order to verify whether it has an apparently biological effects on improving lung injury and survival rate in ARDS. This study aimed to explore the potential value of Foxm1 in the process of BMSC efficiently differentiating into AT II to treat septic ARDS mice, thus to provide theoretical and experimental basis for finding the new treatment methods of ARDS.