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 1-11，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13.9%；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 airway epithelial cells (16HBEs) under benzopyrene (BaP) exposure was established. The ginseng leaf polyphenols (GLPs) were isolated in an activity tracking method with an in vitro model and the protective effect and potential mechanism of the GLP-8 (Albaspidin AA) against inflammation were explored. Intracellular ROS level and epithelial cytokines were evaluated with enzyme linked immunosorbent assay kits. Expression of proteins in aromatic hydrocarbon receptor (AhR) signaling and NLRP3 inflammasome was detected with western blotting. Eventually, eleven GLPs were isolated and their structures were identified. Among them,GLP-8 performed the best protective activity against BaP-induced cell viability decrease. In present study, the BaP-induced ROS secretion was decreased by 19.30% (GLP-8, 5 μg/mL) and 41.30% (GLP-8, 25 μg/mL), respectively. The BaP-induced cell apoptosis was attenuated by 5.80% (GLP-8, 5 μg/mL) and 9.30% (GLP-8, 25 μg/mL), respectively. GLP-8 inhibited The BaP-induced inflammatory factors over-expression was also attenuated. After GLP-8 treatment (25 μg/mL), the IL-33, IL-25, IL-1 β and IL-6 levels were decreased by 60.10%, 28.90%, 33.50% and 41.90%, when compared to the BaP group. Furthermore, the activation of AhR and NLRP3 signal pathway were also suppressed by the GLP-8. Notably, our findings highlighted that GLP-8 could restore the redox homeostasis disrupted by BaP through inhibiting inflammatory factors expression and blocking the AhR/NLRP3 signaling pathway in the airway epithelial cells.

国家自然科学基金项目（面上项目，重点项目，重大项目）