摘要
目的:检测肥胖及牙周炎状态下大鼠骨髓间充质干细胞(BMSCs)及牙髓间充质干细胞(DPSCs)增殖、矿化及成骨能力的变化。方法:分离培养肥胖和牙周炎大鼠的BMSCs和DPSCs,并诱导其骨向分化。以正常大鼠来源的细胞为对照,检测细胞增殖活性及ALP水平,茜素红染色观察矿化结节形成情况,分别检测两种干细胞成骨细胞标志蛋白及RUNT相关转录因子2(Runx2)、骨桥蛋白(OPN)和骨钙蛋白(OCN)的基因和蛋白表达。结果:牙周炎和肥胖均会造成大鼠干细胞细胞增殖加快,细胞矿化能力降低,同时下调多个与成骨相关的基因及蛋白水平。牙周炎合并肥胖会增强上述作用。肥胖对BMSCs的影响大于对DPSCs的影响,而牙周炎对DPSCs的影响大于对BMSCs的影响。结论:肥胖和牙周炎均可增强干细胞增殖、抑制矿化及成骨潜能。
Objective:To study the proliferation activity and osteogenic potential of rat bone marrow stromal stem cells(BMSCs)and dental pulp stem cells(DPSCs)under obese and periodontitis status.Methods:BMSCs and DPSCs from the SD rats with obesity(OB)and periodontitis(PD)were in vitro cultured and osteogenic induced,the cells from normal rats were used as the controls.MTT assay,relative ALP level and alizarin red staining were performed.Osteogenesis related genes and Runt-related transcription factor 2(Runx2),osteopontin(OPN)and osteocalcin(OCN)were detected by qRT-PCR and Western blot analysis.Results:The proliferation of BMSCs and DPSCs from the rats with OB or PD was increased and the mineralization decreased,the levels of multiple genes and proteins related to osteogenesis were down regulated.PD combined with OB aggravated the effects on the cells.OB showed a greater impact on BMSCs than on DPSCs,while PD showed a greater impact on DPSCs than on BMSCs.Conclusion:Both obesity and periodontitis may inhibit proliferation,mineralization and osteogenic potential of stem cells.
作者
于寰
董庭妍
康健
YU Huan;DONG Tingyan;KANG Jian(Department of Periodontology,TianJin Stomatological Hospital/Nankai University Stomatological Hospital,Tianjin Key Laboratory of Oral and Maxillofacial Function Reconstruction,300041,China;Hexi Branch,TianJin Stomatological Hospital/Nankai University Stomatological Hospital,Tianjin Key Laboratory of Oral and Maxillofacial Function Reconstruction,300041,China)
出处
《实用口腔医学杂志》
CAS
CSCD
北大核心
2023年第6期730-737,共8页
Journal of Practical Stomatology
基金
天津市口腔医院博硕士重点项目(编号:2019BSZD08)
天津市口腔医院牙周重点学科建设项目(编号:2022P04)。
关键词
间充质干细胞
肥胖
牙周炎
炎症微环境
Mesenchymal stem cells
Obesity
Periodontitis
Inflammatory microenvironment