Ginseng Leaf Polyphenol-8 (GLP-8) Inhibits BaP-induced Over-expression of Inflammatory Factors in the Airway Epithelial Cells through Regulating the AhR/NLRP3 Signaling Pathway
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Abstract:
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.
