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  

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

作　　者：左志刚[1] 李洪发[1] 王悦[1] 郑朝[1] 杨子靓 刘珊 刘大勇[3] ZUO Zhigang;LI Hongfa;WANG Yue;ZHENG Zhao;YANG Ziliang;LIU Shan;LIU Dayong(Department of Orthodontics, Stomatological Hospital, Tianjin Medical University, Tianjin 300070, China;Tianjin Institute of Cardiovascular Diseases, Tianjin 300222, China;Department of Endodontics, Stomatological Hospital, Tianjin Medical University, Tianjin 300070, China.)

机构地区：[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

出　　处：《口腔医学研究》2020年第11期1069-1073,共5页Journal of Oral Science Research

基　　金：国家自然科学基金(编号:81670953)。

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。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.

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 

分 类 号：R78[医药卫生—口腔医学]