A N Yuanyuan, Liu Wang, L I Yanjie, Wang Yanchun, Ren Xiaobin, H E Hongbing
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引用次数: 0
Abstract
Objective: To investigate the effect and mechanism of Sanqi (Radix Notoginseng) in treating periodontitis.
Methods: The active components and periodontitis targets were analyzed through network pharmacology and molecular docking. A rat model of periodontitis was established and rats were treated by continuous intragastric administration of Sanqi (Radix Notoginseng) at different doses for 30 d. The alveolar bone structure was observed by micro-CT, the periodontal tissue structure was observed by hematoxylin-eosin staining, and the related proteins changes was detected by immunohistochemical staining.
Results: Sanqi (Radix Notoginseng) and periodontitis had a total of 96 coincident targets that were significantly enriched in the interleukin 17 (IL-17), tumor necrosis factor (TNF), and advanced glycation endproducts and the receptor of advanced glycation endproducts signaling pathways. The active compound quercetin had good binding activity with interleukin 6 (IL-6), vascular endothelial growth factor A (VEGFA), matrix metallopeptidase 9 (MMP9), tumor necrosis factor α (TNF-α), Jun proto-oncogene (JUN), and C-X-C motif chemokine ligand 8 (CXCL8) in periodontitis. Compared with normal group, the distance from the cementoenamel junction (CEJ) to the alveolar bone (AB) was increased, alveolar bone absorption was obvious, the periodontal tissue structure was disorganized, and IL-6 and TNF-α were upregulated in periodontitis group; meanwhile, the distance from CEJ to AB was significantly decreased, alveolar bone resorption was reduced, periodontal tissue structure was improved, the expression of IL-6, TNF-α, IL-17 and retinoid-ralated orphan receptor γt (RORγt) were decreased, Forkhead Box P3 (FOXP3) and IL-10 were increased after Sanqi (Radix Notoginseng) treatment.
Conclusions: Sanqi (Radix Notoginseng) improves the structure of alveolar bone and gum, and reduces inflammation; the mechanism involve in inhibiting IL-17 signaling pathway to suppress Th17 and promote Treg cells differentiation.
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