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[通过调节分叉盒蛋白O-1/β-catenin通路对过氧化诱导的人类牙带干细胞的保护作用]

Li Zhang^1,2, Shiyuan Peng^1,2, Feiyang Tang²

¹Dept. of Orthodontics, The Affiliated Stomatological Hospital of Southwest Medical University, Luzhou 646000, China.

Hua xi kou qiang yi xue za zhi = Huaxi kouqiang yixue zazhi = West China journal of stomatology

|September 3, 2025

概括

通过FOXO1/β-catenin通路增强抗氧化能力和恢复骨质生成潜力,保护人类牙带干细胞 (hPDLSCs).

科学领域:

生物材料科学
干细胞生物学
复原医学

背景情况:

氧化应激会影响人类牙周带干细胞 (hPDLSC) 的骨质分化.
一种天然的黄胺 (Naringenin,NAR) 正在研究其潜在的保护作用.

研究的目的:

在氧化应激下研究纳灵 (NAR) 对人类牙周带干细胞 (hPDLSCs) 的骨质生成潜力的保护作用.
阐明涉及FOXO1/β-catenin信号通路的潜在机制.

主要方法:

使用过氧化 (H2O2) 对hPDLSC进行了氧化损伤.
用不同度的NAR和FOXO1抑制剂 (AS1842856) 对细胞进行治疗.
评估了骨质分化,氧化应激标志物 (ROS,MDA,LDH) 和关键蛋白/基因表达 (FOXO1,β-catenin).

主要成果:

在hPDLSC中,H2O2暴露增加了氧化损伤并降低了骨质性潜力.
NAR治疗减轻了氧化损伤,增强了抗氧化能力,并恢复了骨质生成能力.
抑制FOXO1降低了NAR的保护作用,表明该途径的参与.

结论:

纳灵 (NAR) 保护hPDLSCs免受氧化压力引起的损伤.
通过激活FOXO1/β-catenin信号通路,NAR增强了抗氧化能力并恢复了骨质生成潜力.
这突显了NAR作为牙周再生的潜在治疗剂.

关键词:

叉头盒蛋白O-1/β-catenin信号通路类药物骨质的分化氧化应激牙周带干细胞

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