气道炎症所致气道重塑是慢性阻塞性肺疾病（COPD）的重要病理机制。肺表面活性蛋白D（SPD）是调节气道炎症重要的分子。课题组预研结果表明，大气细颗粒物（PM2.5）可抑制SPD的合成和分泌；红景天甙干预后肺组织SPD表达上调，PM2.5引起的气道炎症得到改善。但SPD在PM2.5诱导的气道重塑中的作用尚无报道，红景天甙是否通过促进SPD表达改善PM2.5诱导的气道炎症及重塑也有待研究。本项目拟建立PM2.5诱导的COPD气道重塑小鼠模型并进行红景天甙干预，观察红景天甙在改善PM2.5诱导的COPD模型中的作用。通过siRNA下调II型肺泡上皮细胞SPD的表达，采用流式细胞术、免疫共沉淀等分子生物学技术，探讨红景天甙促进SPD表达改善PM2.5诱导的COPD气道重塑的作用机制。本项目将为PM2.5诱导的COPD防治靶点的探寻提供实验依据，为大气污染导致肺脏损伤的中医药防治提供重要思路。

Airway remodeling caused by airway inflammation is an important pathological mechanism of chronic obstructive pulmonary disease (COPD). Pulmonary surfactant protein D (SPD) is an essential molecule that regulates airway inflammation. The preliminary research results show that atmospheric fine particulate matter (PM2.5) can inhibit the synthesis and secretion of SPD, and salidroside intervention up-regulate the expression of SPD in lung tissue, alleviating airway inflammation caused by PM2.5. However, the role of SPD in PM2.5-induced airway remodeling has not been reported, and whether salidroside alleviate PM2.5-induced airway inflammation and remodeling by promoting SPD expression remains to be studied. This project intends to establish a mouse model of COPD airway remodeling induced by PM2.5 and perform salidroside intervention to observe the effect of salidroside in the PM2.5 induction COPD model. Down-regulated SPD expression of type II alveolar epithelial cells by siRNA, using flow cytometry, immunoprecipitation and other molecular biological techniques to explore the mechanism of salidroside promoting SPD expression and improving PM2.5-induced COPD airway remodeling. This project will provide experimental evidence for the exploring of prevention targets for COPD induced by PM2.5, and provide important ideas for the prevention of lung injury caused by air pollution in Chinese medicine.