Effect and mechanism of Sanqi (Radix Notoginseng) in treating periodontitis

doi:10.19852/j.cnki.jtcm.20241111.001

Abstract

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.

Key words: Sanqi (Radix Notoginseng), periodontitis, quercetin, interleukin-17, inflammationSupporting information

AN Yuanyuan, LIU Wang, LI Yanjie, WANG Yanchun, REN Xiaobin, HE Hongbing. Effect and mechanism of Sanqi (Radix Notoginseng) in treating periodontitis[J]. Journal of Traditional Chinese Medicine, 2025, 45(1): 66-75.

Figures/Tables 4

Figure 1 Regulatory network of common targets in Sanqi (Radix Notoginseng) and periodontitis A: Venn diagram showing overlapping targets of periodontitis and Sanqi (Radix Notoginseng); B: TCM-compound-target-disease network of core targets; C: disease-target-pathway network of core targets. The active ingredient of Sanqi (Radix Notoginseng), quercetin, exhibits the greatest correlation and the most binding nodes with the common targets. DFV: liquiritigenin; Diop: diiso-propyl adipate; FOS: Fos proto-oncogene, AP-1 transcription factor sub-unit; COL3A1: collagen type III alpha 1 chain; MMP3: matrix metallo-pep-tidase 3; MAPK1: mitogen-activated protein kinase 1; CASP1: caspase 1; EGFR: epidermal growth factor receptor; CASP9: caspase 9; ESR1: estrogen receptor 1; RUNX2: runt-related transcription factor 2; NR1I2: nuclear receptor subfamily 1 group I member 2; COL1A1: col-lagen type I alpha 1 chain; ELK1: ETS trans-cription factor ELK1; ADRB2: adr-enoceptor beta 2; HSPB1: heat shock protein family B (small) member 1; IL10: interleukin 10; VCAM1: vascular cell adhesion molecule 1; PLAT: plas-minogen acti-vator, tissue type; PARP1: poly (ADP-ribose) poly-merase 1; IFNG: interferon gamma; SELE: selectin E; MMP9: matrix metallopeptidase 9; MMP1: matrix metallopeptidase 1; AKT1: AKT serine/threonine kinase 1; PTGS1: prostaglandin-endoperoxide synthase 1; NCF1: neutrophil cytosolic factor 1; BCL2L1: BCL2 like 1; ICAM1: intercellular adhesion molecule 1; MPO: myeloperoxidase; CYP1A1: cytochrome P450 family 1 subfamily A member 1; NCOA2: nuclear receptor coactivator 2; MYC: MYC proto-oncogene, BHLH transcription factor; CXCL8: C-X-C motif chemokine ligand 8; EIF6: eukaryotic translation initiation factor 6; NCOA1: nuclear receptor coactivator 1; HAS2: hyaluronan synthase 2; SPP1: secreted phosphoprotein 1; CXCL10: C-X-C motif chemokine ligand 10; IL6: interleukin 6; IL1A: interleukin 1 alpha; SLC6A4: solute carrier family 6 member 4; PTGER3: prostaglandin E receptor 3; CCL2: C-C motif chemokine ligand 2; PPARA: peroxisome proliferator activated receptor alpha; VEGFA: vascular endothelial growth factor A; F3:coagulation factor Ⅲ, tissue factor; IL2: interleukin 2; TP53: tumor protein P53; BAX: BCL2 associated X, apoptosis regulator; TOP2A: DNA topoisomerase Ⅱ alpha; IL1B: interleukin 1 beta; CASP8: caspase 8; CYP1B1: cytochrome P450 family 1 subfamily B member 1; F7: coagulation factor Ⅶ; STAT1: signal transducer and activator of transcription 1; CCND1: cyclin D1; THBD: thrombomodulin; HMOX1: heme oxygenase 1; CHUK: component of inhibitor of nuclear factor kappa B kinase complex; NFE2L2: NFE2 like BZIP transcription factor 2; CTSD: cathepsin D; ADRB1: adrenoceptor beta 1; MMP2: matrix metallopeptidase 2; PRKCA: protein kinase C alpha; GSTM1: glutathione S-transferase Mu 1; SOD1: superoxide dismutase 1; EGF: epidermal growth factor; JUN: Jun proto-oncogene, AP-1 transcription factor subunit; CXCL2: C-X-C motif chemokine ligand 2; SLC2A4: solute carrier family 2 member 4; CXCL11: C-X-C motif chemokine ligand 11; RELA: RELA proto-oncogene, NF-KB subunit; CD40LG: CD40 ligand; BIRC5: baculoviral IAP repeat containing 5; AR: androgen receptor; PSMG1: proteasome assembly chaperone 1; CASP3: caspase 3; NR1I3: nuclear receptor subfamily 1 group I member 3; CAV1: caveolin 1; IGFBP3: insulin like growth factor binding protein 3; PON1: paraoxonase 1; ERBB2: Erb-B2 receptor tyrosine kinase 2; HIF1A: hypoxia inducible factor 1 subunit alpha; GJA1: gap junction protein alpha 1; CDKN1A: cyclin dependent kinase inhibitor 1A; PGR: progesterone receptor; PTGS2: prostaglandin-endoperoxide synthase 2; TNF: tumor necrosis factor; PLAU: plasminogen activator, urokinase; CHEK2: checkpoint kinase 2; ODC1: ornithine decarboxylase 1; NOS3: nitric oxide synthase 3; PPARG: peroxisome proliferator activated receptor gamma; RXRA: retinoid X receptor alpha; IGF2: insulin like growth factor 2; BCL2: BCL2 apoptosis regulator; SERPINE1: serpin family E member 1.

Figure 2 Molecular docking results of the Sanqi (Radix Notoginseng) composition and periodontitis targets A: quercetin + IL6; B: quercetin + VEGFA; C: quercetin + MMP9; D: quercetin + TNF; E: quercetin + JUN; F: quercetin + CXCL8. Yellow objects represent molecular targets, and the surrounding chain represents the compound. IL6: interleukin 6; VEGFA: vascular endothelial growth factor A; MMP9: matrix metallopeptidase 9; TNF: tumor necrosis factor; JUN: Jun proto-oncogene; AP-1 transcription factor subunit; CXCL8: C-X-C motif chemokine ligand 8.

Figure 3 Sanqi (Radix Notoginseng) improved periodontal tissue structure in rats with periodontitis A: micro-CT was used to observe effects of Sanqi (Radix Notoginseng) on the morphology and structure of alveolar bone; B: statistical analysis of the distance from the cementoenamel junction (CEJ) to the alveolar bone (AB) (n = 3); C: Hematoxylin eosin staining was performed to observe the changes of periodontal tissue structure after Sanqi (Radix Notoginseng) treatment (Scale bar = 500 μm, × 2) (n = 3). A1, C1: Normal group; A2, C2: Periodontitis group; A3, C3: Low-dose group; A4, C4: Middle-dose group; A5, C5: High-dose group. Normal group: normal rats were intragastric with solvent; Periodontitis group: periodontitis rats were intragastric with solvent; Low-dose group: periodontitis rats were intragastric with Sanqi (Radix Notoginseng) (0.625 g/kg); Middle-dose group: periodontitis rats were intragastric with Sanqi (Radix Notoginseng) (1.25 g/kg); High-dose group: periodontitis rats were intragastric with Sanqi (Radix Notoginseng) (2.5 g/kg). Student t-test and one-way analysis of variance were performed for the normal, periodontitis, and Sanqi (Radix Notoginseng) treatment group comparisons analysis, and data were presented as mean ± standard deviation (n = 3). Compared with the normal group, aP < 0.05; compared with the periodontitis group, bP < 0.05.

Figure 4 Sanqi (Radix Notoginseng) regulated the expression of inflammation-related factors A: immunohistochemical staining was used to detect the expression of IL-6, TNF-α, IL-17, RORγt, FOXP3, and IL-10 in local periodontal tissues (scale bar = 10 μm, × 150). A1-A5: IL-6; A6-A10: TNF-α; A11-A15: IL-17; A16-A20: RORγt; A21-A25: FOXP3; A26-A30: IL-10. A1, A6, A11, A16, A21, A26: Normal group; A2, A7, A12, A17, A22, A27: Periodontitis group; A3, A8, A13, A18, A23, A28: Low-dose group; A4, A9, A14, A19, A24, A29: Middle-dose group; A5, A10, A15, A20, A25, A30: High-dose group; B: statistical analysis of IL-6 expression changes in each group; C: statistical analysis of TNF-α expression changes in each group; D: statistical analysis of IL-17 expression changes in each group; E: statistical analysis of RORγt expression changes in each group; F: statistical analysis of FOXP3 expression changes in each group; G: statistical analysis of IL-10 expression changes in each group. Normal group: normal rats were intragastric with solvent; Periodontitis group: periodontitis rats were intragastric with solvent; Low-dose group: periodontitis rats were intragastric with Sanqi (0.625 g/kg); Middle-dose group: periodontitis rats were intragastric with Sanqi (1.25 g/kg); High-dose group: periodontitis rats were intragastric with Sanqi (2.5 g/kg). IL-6: interleukin 6; TNF-α: tumor necrosis factor α; IL-17: interleukin 17; RORγt: retinoid-ralated orphan receptor γt; FOXP3: Forkhead Box P3; IL-10: interleukin 10. Student t-test and one-way analysis of variance were performed for the normal, periodontitis, and Sanqi (Radix Notoginseng) treatment group comparisons analysis and data were presented as mean ± standard deviation (n = 3). Compared with the normal group, aP < 0.05; compared with the periodontitis group, bP < 0.05.

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