本文研究了苯并芘（Bap）诱发肺上皮细胞炎性损伤的作用机制及陈皮中的酚类化合物的抗炎活性及作用机制。通过从陈皮中分离出来酚类化合物并用于抗Bap诱导的人肺上皮II型细胞（A549）损伤的活性研究，检测Bap对细胞炎症因子、NF-κB、芳基烃受体（AHR）通路相关蛋白表达的影响及陈皮酚类化合物对Bap造成损伤的保护作用。本文从陈皮中分离得到6个酚类化合物，研究表明，其中aspidin BB可降低3.74%由Bap诱导的A549细胞凋亡。aspidin BB可抑制Bap诱导的NO及炎症因子（IL-1β、IL-6和TNF-α）分泌，分别降低了49.22%、26.79%、37.86%和42.94%。Western blotting结果显示，aspidin BB可抑制Bap诱导的AHR和NF-κB相关蛋白的激活，增强A549细胞的抗炎作用。因此得出陈皮酚类化合物aspidin BB可通过减少Bap诱导的炎性因子分泌，调控AHR、NF-κB通路发挥抗炎及抗氧化损伤的功能。

To study the mechanism of benzo-α-pyrene (Bap) induced inflammatory injury in pulmonary epithelial cells and explore the protective effect of pericarpium citri reticulatae phenolics, the phenolics in pericarpium citri reticulatae was isolated and their anti-inflammatory potency in Bap induced human lung epithelial type II cells (A549) was explored. The expressions of inflammatory factors and the protein expression in NF-κB, aryl hydrocarbon receptor (AHR) pathways were detected, and the protective potency of the phenolics was explored. Six phenolics were isolated and their structures were identified, among whichaspidin BB can reduce by 3.74% apoptosis in Bap-induced A549 cell. Further, aspidin BB inhibited the secretion of NO and the inflammatory factors (IL-1β, IL-6 and TNF-α) by 49.22%, 26.79%, 37.86% and42.94% respectively. Western blotting results showed that aspidin BB significantly inhibited the activation of AHR and NF-κB pathways induced by Bap stimuli. The phenolics isolated from the pericarpium citri reticulatae can regulate the AHR and NF-κB pathways to attenuate the inflammatory and oxidant damages induced by the Bap stimuli.