口腔医学研究

口腔医学研究 ›› 2020, Vol. 36 ›› Issue (11): 1069-1073.DOI: 10.13701/j.cnki.kqyxyj.2020.11.019

• 口腔正畸学研究 • 上一篇    下一篇

SIRT1对正畸静压力刺激下牙周膜干细胞成骨分化的调控作用及机制

左志刚1, 李洪发1, 王悦1, 郑朝1, 杨子靓1, 刘珊2, 刘大勇3*   

  1. 1.天津医科大学口腔医院正畸科 天津 300070;
    2.天津市心血管病研究所 天津 300222;
    3.天津医科大学口腔医院牙体牙髓科 天津 300070
  • 收稿日期:2020-02-22 出版日期:2020-11-28 发布日期:2020-11-27
  • 通讯作者: *刘大勇,E-mail:dayongliutj@163.com
  • 作者简介:左志刚(1982~ ),男,河北张家口人,硕士,主治医师,研究方向:正畸牙齿移动生物学及生物力学。
  • 基金资助:
    国家自然科学基金(编号:81670953)

Regulation and Mechanism of SIRT1 on Osteogenic Differentiation of Periodontal Ligament Stem Cells Stimulated by Orthodontic Static Pressure

ZUO Zhigang1, LI Hongfa1, WANG Yue1, ZHENG Zhao1, YANG Ziliang1, LIU Shan2, LIU Dayong3*   

  1. 1. Department of Orthodontics, Stomatological Hospital, Tianjin Medical University, Tianjin 300070, China;
    2. Tianjin Institute of Cardiovascular Diseases, Tianjin 300222, China;
    3. Department of Endodontics, Stomatological Hospital, Tianjin Medical University, Tianjin 300070, China
  • Received:2020-02-22 Online:2020-11-28 Published:2020-11-27

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摘要： 目的:研究沉默信息调节因子1(SIRT1)对正畸静压力刺激下牙周膜干细胞(PDLSCs)成骨分化的调控作用及机制。方法:原代培养PDLSCs,取第3代PDLSCs并分为对照组、正畸静压力组、正畸静压力+白藜芦醇组、正畸静压力+烟酰胺组,检测SIRT1、骨钙素(OCN)、RUNT相关转录因子2(RUNX2)、乙酰化NF-κB、FOXO1、乙酰化FOXO1的表达量及肿瘤坏死因子-α(TNF-α)、白细胞介素-6(IL-6)、单核细胞趋化蛋白-1(MCP-1)的含量,成骨诱导后检测茜素红染色中矿化结节数量。结果:与对照组比较,正畸静压力组的矿化结节数量、SIRT1、OCN、RUNX2、FOXO1的表达量增加,乙酰化NF-κB、乙酰化FOXO1的表达量及TNF-α、IL-6、MCP-1的含量减少;与正畸静压力组比较,正畸静压力+白藜芦醇组的矿化结节数量、SIRT1、OCN、RUNX2、FOXO1的表达量增加,乙酰化NF-κB、乙酰化FOXO1的表达量及TNF-α、IL-6、MCP-1的含量减少,正畸静压力+烟酰胺组的矿化结节数量、SIRT1、OCN、RUNX2、FOXO1的表达量减少,乙酰化NF-κB、乙酰化FOXO1的表达量及TNF-α、IL-6、MCP-1的含量增加。结论:SIRT1在正畸静压力刺激下PDLSCs成骨分化中起促进作用,调控NF-κB及FOXO1的乙酰化是其可能的分子机制。

关键词: 牙周膜干细胞, 沉默信息调节因子1, 成骨分化, 乙酰化

Abstract: Objective: To study the effect and mechanism of SIRT1 on osteogenic differentiation of PDLSCs stimulated by orthodontic static pressure. Methods: Primary PDLSCs were cultured and the third generation of PDLSCs was divided into control group, orthodontic static pressure group, orthodontic static pressure+resveratrol group, and orthodontic static pressure+nicotinamide group. The expression of SIRT1, OCN, Runx2, acetylated NF-κB, FOXO1, acetylated FOXO1, and the contents of TNF-α, IL-6, and MCP-1 were measured. The mineralized nodules numbers of alizarin red staining after osteogenesis induction were detected. Results: Compared with the control group, the number of mineralized nodules and the expression of SIRT1, OCN, Runx2, and FOXO1 increased, the expression of acetylated NF-κB, acetylated FOXO1, and the contents of TNF-α, IL-6, and MCP-1 decreased in orthodontic static pressure group. Compared with orthodontic static pressure group, the number of mineralized nodules and the expression of SIRT1, OCN, Runx2, and FOXO1 increased; the expression of acetylated NF-κB, acetylated FOXO1, and the contents of TNF-α, IL-6, and MCP-1 decreased in orthodontic static pressure+resveratrol group; the number of mineralized nodules and the expression of SIRT1, OCN, Runx2, and FOXO1 decreased; the expression of acetylated NF-κB, acetylated FOXO1, and the contents of TNF-α, IL-6, and MCP-1 increased in orthodontic static pressure+nicotinamide group. Conclusion: SIRT1 plays an important role in the osteogenic differentiation of PDLSCs under the stimulation of orthodontic static pressure, and its possible molecular mechanism is to regulate the acetylation of NF-κB and FoxO1.

Key words: periodontal ligament stem cells, silent information regulator 1, osteogenic differentiation, acetylation