基于活性追踪方法分离人参叶多酚化合物（Ginseng leaf polyphenols，GLPs)并研究其抗环境污染物苯并芘（Benzo(a)pyrene，BaP）诱发气道上皮细胞（16HBE）氧化、炎症损伤的作用机制。最终分离、鉴定11个人参叶多酚化合物GLP-1~ GLP-11，其中GLP-8（Albaspidin AA，Ginseng leaf polyphenol-8）能够显著抑制BaP诱导的16HBE细胞损伤；相比于BaP组，GLP-8使16HBE细胞活力提升13.90%；GLP-8使BaP诱导的活性氧（Reactive oxygen species，ROS）过量分泌分别降低了19.30%（5 μg/mL）和41.30%（25 μg/mL）；GLP-8使Bap诱导的16HBE细胞凋亡率分别降低5.80%（5 μg/mL）和9.30%（25 μg/mL）；25 μg/mL GLP-8作用后，BaP诱导的炎症因子IL-33、IL-25、IL-1β及IL-6的表达分别减少60.10%、28.90%、33.50%及41.90%；GLP-8抑制芳香烃受体（AhR）及核苷酸结合寡聚化结构域样受体蛋白3（NLRP3）信号通路激活。因此得出，GLP-8具有通过调控AhR/NLRP3信号通路抑制BaP诱导的ROS过量分泌及炎症因子过表达来发挥保护气道上皮细胞活性的功能。

Here, a model of under benzopyrene (BaP) exposure was established. The isolation of ginseng leaf polyphenols (GLPs) were performed based on an activity tracking method, and the mechanisms underlying their anti-oxidative and inflammatory effects against environmental pollutant benzo(a)pyrene (BaP)-induced oxidation and inflammatory injury in airway epithelial cells (16HBEs) were studied. Finally, 11 ginseng leaf polyphenol compounds GLP-1~GLP-11 were isolated and identified, of which GLP-8 (Albaspidin AA, Ginseng leaf polyphenol-8) could significantly inhibit BaP-induced 16HBE cell damage; Compared with the BaP group, GLP-8 increased the viability of 16HBE cells by 13.90%; GLP-8 reduced the excessive secretion of reactive oxygen species (ROS) induced by BaP by 19.30% (GLP-8, 5 μg/mL) and 41.30% (GLP-8, 25 μg/mL), respectively. GLP-8 reduced the apoptosis rate of Bap-treated 16HBE cells by 5.80% (GLP-8, 5 μg/mL) and 9.30% (GLP-8, 25 μg/mL), respectively. After the GLP-8 treatment (25 μg/mL), the expressions of BaP-induced inflammatory factors, IL-33, IL-25, IL-1β and IL-6 decreased by 60.10%, 28.90%, 33.50% and 41.90%, respectively; when compared to the BaP group. GLP-8 inhibited the activation of aryl hydrocarbon receptor (AhR) and nucleotide-binding oligomerization domain-like receptor protein 3 (NLRP3) signaling pathways. Therefore, it is concluded that GLP-8 could protect the activities of the airway epithelial cells through regulating the AhR/NLRP3 signaling pathway and inhibiting BaP-induced excessive secretion of ROS and over-expressions of inflammatory factors.

国家自然科学基金项目（31770984；81803202；81929001；81901634）；广东省自然科学基金项目（2020A1515010029；2019A1515110010）；深圳市科技计划项目（KQTD20170331145453160；LHTD20180007）；呼吸疾病国家重点实验室开放项目（SKLRD-OP-201910）；西南医科大学创新课题（20091）