特发性肺纤维化（IPF）致残率高、死亡率高、预后不良，尚缺乏有效疗法。其日益增高的发病率与大气污染加剧密切相关，但相关机制尚不明确。本项目基于“正虚络痹积损”致纤维化的病机理论，以博来霉素（BLM）诱导的IPF大鼠模型和A549、MRC-5细胞模型为对象，并采用PM2.5暴露，采用病理学、激光共聚焦显微镜、qPCR、免疫组化/印迹等技术，研究PM2.5对BLM诱导的IPF大鼠模型的影响特点和机制；并在此基础上观察具有补肺益气、活血化痰通络功用的保肺化纤方对肺组织形态学和羟脯氨酸、活性氧、细胞因子、趋化因子和细胞外基质及A549、MRC-5细胞功能和TGF-β、Wnt/β-catenin信号通路的影响，揭示保肺化纤方的效应特点及其通过调控TGF-β和wnt/β-catenin信号通路调节上皮间质细胞转化的作用机制，为寻求有效治疗手段提供科学依据。

Idiopathic pulmonary fibrosis (IPF) is a severe disease with high rates of disability and mortality, and poor prognosis, without effective therapeutics. Its increasing morbidity has been strongly linked to aggravating air pollution, however, the underlying mechanism remains unclear. Based on the pathogenesis theory coursing fibrosis of vital deficiency, collaterals impediment and impairment accumulation, we aim to use a bleomycin (BLM)-induced IPF rat model and human type II alveolar epithelial cell (A549) and lung fibroblast (MRC-5) models as study objects, and expose the models to air pollutant particulate matter (PM) 2.5. The affecting characters and mechanisms of PM2.5 on the IPF rat model will be determined with pathological, laser scanning confocal microscope, quantitative polymerase chain reaction, immunohistochemical and western blotting methods. Furthermore, we will observe the effects of Baofei Huaxian granules, a traditional Chinese medicine with efficacy of invigorating lung qi, promoting blood circulation and resolving phlegm and dredging collaterals, on pulmonary histomorphology, and productions of hydroxyproline, reactive oxygen species, cytokines, chemokines and extracellular matrix, and the functions of A549 and MRC-5 cells, and TGF-β and Wnt/β-catenin signaling regulation. Through this study, we wish to observe the impact characters of PM2.5 on the BLM-induced IPF rat model, and explore the effective features of Baofei Huaxian granules on regulating epithelial-mesenchymal transition via TGF-β and wnt/β-catenin signaling regulations, and provide scientific basis for searching more beneficial therapeutics.