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作 者:齐东杰 周鑫磊 嵇步云 林家婷 QI Dongjie;ZHOU Xinlei;JI Buyun;LIN Jiating(School of Stomatology,Wannan Medical College,China,241002 Wuhu;Department of Stomatology,the First Affiliated Hospital of Wannan Medical College,Wuhu)
机构地区:[1]皖南医学院口腔医学院,芜湖241002 [2]皖南医学院第一附属医院弋矶山医院口腔科
出 处:《实用口腔医学杂志》2024年第5期647-651,共5页Journal of Practical Stomatology
基 金:安徽高校自然科学研究项目(编号:KJ2020A0617);医院引进人才科研基金(编号:YR202117)。
摘 要:目的:探讨二甲双胍介导高糖高脂环境下大鼠颌骨骨髓间充质细胞(BMSCs)成骨分化机制。方法:体外分离并培养SD大鼠(雄性)下颌骨BMSCs,分为对照组(C组),高糖高脂组(H组),二甲双胍刺激的正常组(CM组),二甲双胍刺激的高糖高脂组(HM组)。EDU染色检测探究二甲双胍对BMSCs增殖的影响;BMSCs经诱导后,用碱性磷酸酶染色、茜素红染色和油红O染色检测细胞成骨分化和成脂分化能力;用Western blot和免疫荧光染色检测BMSCs成骨分化因子runt-相关转录因子2(Runx2)、骨钙素(OCN)的蛋白表达量。结果:HM组较H组比较,细胞增殖能力增强,Runx2、OCN表达水平升高(P<0.05),成骨分化能力显著提高,成脂分化能力显著下降。结论:二甲双胍可诱导BMSCs表达Runx2和OCN,促进体外培养的高糖高脂环境下大鼠颌骨BMSCs增殖与成骨分化。Objective:To explore the mechanism of metformin on osteogenic differentiation of rat jaw bone marrow mesenchymal cells(BMSCs)under high sugar and high fat environment.Methods:BMSCs of male SD rats were isolated and cultured in vitro and divided into 4 groups:Control group(C group),high sugar and high fat group(H group),control cells and H group cells were respectively stimulated with metformin(CM group and HM group).EDU staining was used to detect the cell proliferation;after osteogenesis and adipogenesis induction of BMSCs,alkaline phosphatase staining,alizarin red(O)staining and oil red O staining were respectively used to detect the osteogenic and adipogenic differentiation of the cells.The protein expression of Runx2 and OCN was detected by Western blot and immunofluorescence staining respectively.Results:Compared with the H group,in the HM group the cell proliferation ability was enhanced,the expression levels of Runx2 and OCN were increased(P<0.05),the osteogenic differentiation ability was significantly increased,and the adipogenic differentiation ability was significantly decreased.Conclusion:In vitro,metformin promotes the proliferation and osteogenic differentiation of rat jaw BMSCs cultured with a high sugar and high fat environment by increase of the expression of Runx2 and OCN.
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