急性呼吸窘迫综合征（ARDS）是儿童时期常见的危重病，主要特点是顽固性低氧血症，抢救成功率低。胞红蛋白（CYGB）是新发现的第四种携氧珠蛋白，与组织细胞的氧输送及氧利用有关。本研究以肺和支气管上皮细胞制作低氧细胞模型，用油酸制作幼年小鼠ARDS模型，采用免疫组化、RT-qPCR和Western blot技术，测定肺组织细胞CYGB、钙调神经磷酸酶 (CaN)信号通路蛋白、低氧诱导因子的表达变化，以及肺组织细胞氧化损伤、生长凋亡指标。同时利用质粒转染技术、基因敲入技术、CaN信号通路促进剂，促进CYGB的表达，观察对ARDS组织损伤及修复的影响。本研究通过阐明CYGB在ARDS发病中的作用，从机体氧运输、氧储存和氧利用的角度，探讨ARDS发生低氧血症的可能机制，并通过阐明CYGB表达调控的信号途径，为今后的治疗干预寻找方向。结果也将为其它危重疾病在氧代谢方面的研究奠定坚实的基础。

Acute respiratory distress syndrome (ARDS) is a common critical disease in childhood. It is characterized by refractory hypoxemia and has a low success rate of rescue. Cytoglobin (CYGB) is the fourth newly discovered oxygen-carrying globin, related to oxygen transport and utilization in histocyte. We set up a low-oxygen model of lung and bronchial epithelial cell and a young mice model with ARDS by injecting oleic acid, measuring the expressions of CYGB, calcineurin (CaN) signaling molecules and hypoxia-inducible factor in lung by immunohistochemistry, RT-qPCR or Western blot technique. The markers of oxidative damage and status of growth and apoptosis are also evaluated in cell and animal models. In addition, we utilize plasmid transfection technique, CYGB gene knockin and CaN signal pathway promoters to promote the expression of CYGB, observing the effects on damage or repair in lungs of ARDS model. This study aims to elucidate the effects of CYGB on ARDS and to explore the possible pathogenesis of hypoxemia in ARDS from the point of view of oxygen transport, storage and utilization. We also try to illustrate the signal pathways on how to regulate the CYGB expression in an effort to find the new way for future intervention on ARDS. The study will also lay a solid foundation on the research of oxygen metabolism in other critical diseases.