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Objective @#To explore the medication law and mechanism of traditional Chinese medicine compounds in the treatment of periodontal disease through data mining, network pharmacology, and molecular docking. @* Methods@#First, data mining was used to search single medicinal materials for the treatment of periodontal disease, and the active components and their action targets were screened. Second, the disease target database was employed to download the targets related to the pathogenesis of periodontal disease, map them with the action targets of traditional Chinese medicine, and obtain the targets that are considered potential targets of traditional Chinese medicine in the treatment of periodontal disease. Potential targets were analyzed for gene ontology function and signaling pathway. They were then screened to obtain the key targets for the treatment of periodontal disease. Finally, the active components were docked with key targets.@* Results@# Among the traditional Chinese medicine prescriptions for the treatment of periodontal disease, Shudihuang, Mudanpi, Danggui, Fuling, Jinyinhua, Shanyao and Zhimu had the highest frequencies. Forty-three active components and 118 action targets were screened, and 52 potential targets were obtained by intersection with 856 disease targets. The molecular functions and biological processes in which potential targets may participate mainly focus on vitamin D biosynthesis and RNA polymerase Ⅱ regulation and involve 96 signaling pathways. Through the analysis of network topology parameters, 11 key targets were obtained. The results of molecular docking showed that the active components and RAC-alpha serine/threonine-protein kinase (AKT1), cellular tumor antigen p53 (TP53), and mitogen-activated protein kinase-1 (MAPK-1) have good binding activity. @* Conclusion @#Traditional Chinese medicine compounds may play a role in the treatment of periodontal disease by inhibiting alveolar bone absorption, have antibacterial and anti-inflammatory properties, and promote tissue repair. The effective treatment of periodontal disease by traditional Chinese medicine compounds provides a more scientific reference to the sustainable development of traditional Chinese medicine.
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Objective @#To investigate the effect of different concentrations of MTA on the proliferation and differentiation of stem cells from the apical papilla (SCAP) and the potential of the SCAP to differentiate into odontoblasts.@*Methods@#SCAP were cultured in different concentrations of mineral trioxide aggregate（MTA）. MTA experimental group with concentration of 0.01 mg/mL, 0.02 mg/mL, 0.1 mg/mL, 0.2 mg/mL, 1 mg/mL, 2 mg/mL, 10 mg/mL and 20 mg/mL were prepared. The number of cells at 1 day, 3 days, 5 days and 7 days were measured via a CCK-8 assay to observe the effect of MTA on SCAP proliferation. Real-time PCR was used to detect the gene expression changes. Cells cultured in alpha MEM culture containing 15% FBS without MTA were set as the control group.@*Results @#When cultured for 1 d, statistically significant differences in the promotion of in vitro proliferation of SCAP were not observed between each MTA experimental group and the control group (P>0.05). When cultured for 3 d, 5 d and 7 d, the 0.01 mg/mL MTA group presented obvious promotion of SCAP proliferation compared with the control group (P<0.05), whereas the 0.02 mg/mL, 0.1 mg/mL, 0.2 mg/mL, 1 mg/mL groups did not presented differences with the control group (P>0.05). The in vitro proliferation of the 2 mg/mL, 10 mg/mL and 20 mg/mL groups was lower than that of the control group (P<0.05). Real-time PCR detection showed that the expression levels of DSPP (t=-11.12, P < 0.05) and Runx2 (t=-10.62, P < 0.05) in the experimental group treated with 0.01 mg/mL MTA for 7 days were higher than those in the control group. @*Conclusion @#The 0.01 mg/mL concentration of MTA significantly promotes the proliferation of SCAP and shows the best ability to induce osteogenic and odontoblast differentiation in the SCAP, whereas high concentrations of MTA inhibited the proliferation of SCAP.