Nrf2/ARE通路与COPD氧化/抗氧化失衡密切相关，在前一个国家青年基金的资助下发现:COPD状态下MRP1功能和表达降低，化痰降气方（HTJQF）逆转MRP1功能和表达发挥治疗作用。我们假设：COPD状态下MRP1表达下调是肺上皮细胞Nrf2/ARE通路失活所致，HTJQF通过激活Nrf2/ARE信号通路而调控MRP1表达。采用Nrf2基因敲除小鼠，建立COPD模型，探讨Nrf2/ARE通路在COPD状态下Mrp1表达中作用及其下游相关基因的改变，并以该通路为靶点，结合体外采用siRNA干扰上皮细胞Nrf2表达，研究HTJQF基于激活Nrf2/ARE途径上调Mrp1表达的作用及胞内信号转导机制。其成果对于明确HTJQF上调MRP1的作用机制，了解Nrf2/ARE信号通路在COPD中的作用均有重要意义，亦体现中药复方在治疗COPD中优势，为中医药防治COPD提供新的作用靶点和研究思路。

Nrf2/ARE pathway is closely associated with COPD oxidant / antioxidant imbalance. Our study supported by the National Natural Science Foundation found there was a reduced MRP1 function and expression in COPD, Huatanjiangqifang （HTJQF） up-regulated the reduced function and expression of MRP1 in the lung of COPD to achieve effective treatment COPD. We assume that the down-regulation of MRP1 was due to the inactivated Nrf2/ARE pathway in COPD lung epithelial cells, and HTJQF regulated the MRP1 expression by activating Nrf2/ARE signaling pathways. Applying Nrf2 knockout mice to establish COPD model, we investigate the role of Nrf2/ARE pathway in Mrp1 expression and its downstream related genes in lung, and with the epithelial cells using siRNA interference Nrf2 expression and specific signaling pathway inhibitor in vitro, we research the mechanism of HTJQF up-regulation of Mrp1 expression by activating Nrf2/ARE pathway. The results would contribute to a better understanding of the mechanism of HTJQF up-regulation of Mrp1 expression and the role of Nrf2/ARE pathways in COPD, embody the advantages of traditional chinese medicine (TCM) in the treatment of COPD and provide a new target for TCM on COPD therapy.