我们的前期研究发现细胞色素C氧化酶（COX）Ⅱ的表达及活性下降能激活线粒体凋亡途径，参与COPD肺血管内皮细胞凋亡；并且在COPD人群肺血管内皮细胞中存在Notch1的表达异常，而上调Notch1可部分逆转吸烟COPD动物模型肺血管内皮细胞凋亡。而已有研究发现miRNA34a可能参与COPD的疾病过程，且miRNA34a能够通过Notch1通路调控肿瘤细胞等凋亡。但在COPD肺血管内皮细胞中是否存在miRNA34a经Notch1通路调控COXⅡ的表达及活性有待进一步求证。本研究拟通过在COPD患者、COPD小鼠模型，以及香烟提取物（CSE）干预后的人肺血管内皮细胞中观察miRNA34a、Notch1通路和COXⅡ的改变；从而探讨在COPD的肺血管内皮细胞凋亡中是否存在miRNA34a经Notch1通路调节COXⅡ的机制，为寻找COPD治疗新措施提供理论指导。

Decrease of expression and activity of Cytochrome C oxidase (COX)Ⅱwas found in our previous reasearch. This decreas activate the mitochondria pathway of apoptosis, and take apart in pulmonary endothelia apoptosis of COPD. We also found downregulation Notch1 in pulmonary endothelia of COPD patients，and overexpression of Notch1 could partly reverse endothelia apoptosis. Furthermore, miRNA34a could regulate tumor cell apoptosis through Nothc1 pathway, and there is a deregulation of miRNA34a in COPD lung tissue. There is a need to ivestigate whether there is a deregulation of miRNA34a, which could decrease the expression and activity of COXⅡthrough Notch1 pathway in pulmonary endothelia apoptosis of COPD. This study will observe the changes of miRNA34a, Notch1 pathway and COXⅡin COPD patients, models and endothelium treated with CSE, to investigate whether there is deregulation of miRNA34a, which could decrease the expression and activity of COXⅡthrough Notch1 pathway in pulmonary endothelia apoptosis of COPD.