黄芪甲苷调节人牙周膜细胞炎症反应及成骨分化的作用及机制研究

doi:10.13701/j.cnki.kqyxyj.2020.02.008

口腔医学研究 ›› 2020, Vol. 36 ›› Issue (2): 121-125.DOI: 10.13701/j.cnki.kqyxyj.2020.02.008

黄芪甲苷调节人牙周膜细胞炎症反应及成骨分化的作用及机制研究

王素文^*, 赖思煜, 习利军, 王利宏

广州中医药大学深圳医院(福田)口腔科广东深圳 518110

收稿日期:2019-06-06 出版日期:2020-02-28 发布日期:2020-04-24
通讯作者: 王素文,E-mail: 124397454@qq.com
作者简介:王素文(1979~ ) ,女,汉族,内蒙古人,硕士,研究方向:牙周炎。
基金资助:
2018年深圳市卫生公益科研项目(编号:FTWS2018061)

Effect and Mechanism of Astragaloside on Regulating the Inflammatory Response and Osteogenic Differentiation of Human Periodontal Ligament Cells

WANG Suwen^*, LAI Siyu, XI Lijun, WANG Lihong

Department of Stomatology, Affiliated Hospital of Shenzhen (Futian), Guangzhou University of Chinese Medicine, Shenzhen 518110, China

Received:2019-06-06 Online:2020-02-28 Published:2020-04-24

摘要/Abstract

摘要： 目的:观察黄芪甲苷调节人牙周膜细胞(human periodontal ligament cells,hPDLCs)炎症反应及成骨分化的作用及机制。方法:原代培养hPDLCs后消化传代,取第3代hPDLCs并分为对照组、感染组、黄芪甲苷组、黄芪甲苷+含NLR家族Pyrin域蛋白3(NLR family, pyrin domain containing 3,NLRP3)过表达组。检测白细胞介素(interleukin,IL)-1β、IL-18、碱性磷酸酶(alkaline phosphatase,ALP)、NLRP3、含半胱氨酸的天冬氨酸蛋白水解酶-1(cysteinyl aspartate specific proteinase-1,Caspase-1)、Runt2相关转录因子2(Runt-related transcription factor 2,RUNX2)、骨桥蛋白(osteopontin,OPN),矿化诱导后进行茜素红染色,观察矿化结节。结果:黄芪甲苷组培养基中IL-1β、IL-18的含量及细胞中IL-1β、IL-18、NLRP3、Caspase-1的表达量明显低于感染组,培养基中ALP的活力、细胞中RUNX2及OPN的表达量、矿化结节数目均高于感染组;黄芪甲苷+NLRP3过表达组培养基中IL-1β、IL-18的含量及细胞中IL-1β、IL-18、NLRP3、Caspase-1的表达量明显高于黄芪甲苷组,培养基中ALP的活力、细胞中RUNX2及OPN的表达量、矿化结节数目均低于黄芪甲苷组。结论:黄芪甲苷能够通过抑制NLRP3炎症小体的激活来抑制牙龈卟啉单胞菌感染hPDLCs的炎症反应并促进成骨分化。

关键词: 牙周膜细胞, 牙龈卟啉单胞菌, 黄芪甲苷, 含NLR家族Pyrin域蛋白3炎症小体, 炎症反应, 成骨分化

Abstract: Objective: To observe the effect and mechanism of astragaloside on regulating the inflammatory response and osteogenic differentiation of human periodontal ligament cells (hPDLCs) infected by Porphyromonas gingivalis through NLRP3 inflammasome. Methods: Primary hPDLCs were cultured and digested, and the third generation of hPDLCs was divided into control group, infection group, astragaloside group, astragaloside+ NLR family, and pyrin domain containing 3 (NLRP3) overexpression group. Interleukin (IL)-1β, IL-18, alkaline phosphatase (ALP), NLRP3, cysteinyl aspartate specific proteinase-1 (Caspase-1), Runt-related transcription factor (RUNX2), and osteopontin (OPN) in cells were detected. Alizarin red staining was performed after mineralization induction to observe the mineralized nodules. Results: The contents of IL-1β and IL-18 in the culture medium and the expressions of IL-1β, IL-18, NLRP3, and Caspase-1 in the cells of the astragaloside group were significantly lower than those of the infection group. The activity of ALP in the culture medium, the expression of RUNX2 and OPN in the cells, and the number of mineralized nodules were higher than those of the infection group. The contents of IL-1β and IL-18 in the culture medium and the expressions of IL-1β, IL-18, NLRP3, and Caspase-1 in the cells of astragaloside+NLRP3 overexpression group were significantly higher than those of the astragaloside group. The activity of ALP in the culture medium, the expressions of RUNX2 and OPN in the cells, and the number of mineralized nodules were lower than those of the astragaloside group. Conclusion: Astragaloside can inhibit the inflammatory response of porphyromonas gingivalis infected hPDLCs and promote the osteogenic differentiation by inhibiting the activation of NLRP3 inflammasome.

Key words: periodontal ligament cells, porphyromonas gingivalis, astragaloside, NLR family, pyrin domain, containing 3 inflammasome, inflammatory response, osteogenic differentiation

王素文, 赖思煜, 习利军, 王利宏. 黄芪甲苷调节人牙周膜细胞炎症反应及成骨分化的作用及机制研究[J]. 口腔医学研究, 2020, 36(2): 121-125.

WANG Suwen, LAI Siyu, XI Lijun, WANG Lihong. Effect and Mechanism of Astragaloside on Regulating the Inflammatory Response and Osteogenic Differentiation of Human Periodontal Ligament Cells[J]. Journal of Oral Science Research, 2020, 36(2): 121-125.

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黄芪甲苷调节人牙周膜细胞炎症反应及成骨分化的作用及机制研究

Effect and Mechanism of Astragaloside on Regulating the Inflammatory Response and Osteogenic Differentiation of Human Periodontal Ligament Cells

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