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在糖尿病相关的牙周炎中,SIRT3通过脱乙LRPPRC来缓解线粒体功能障碍和衰老

Hui Tang¹, Yi Zhou¹, Lu Ma¹

¹Department of Periodontology, The Affiliated Stomatological Hospital of Nanjing Medical University, Nanjing, China; State Key Laboratory Cultivation Base of Research, Prevention and Treatment for Oral Diseases, Nanjing Medical University, Nanjing, China; Jiangsu Province Engineering Research Center of Stomatological Translational Medicine, Nanjing, China.

Free radical biology & medicine

|November 18, 2024

概括

糖尿病相关的牙周炎通过抑制SIRT3.3来加速人类牙周干细胞的衰老. 用Honokiol激活SIRT3,延缓衰老并促进骨再生,为这种疾病提供了一个新的治疗点.

科学领域:

生物医学科学生物医学科学
干细胞生物学干细胞生物学
牙周病学牙周病学

背景情况:

糖尿病相关牙周炎 (DP) 是一种导致牙损失的炎症性疾病.
在DP的慢性炎症诱导人类牙周干细胞 (hPDLSCs) 的衰老,损害了它们的功能.
锡图因3 (SIRT3) 是一种依赖NAD+的脱乙酶,参与了衰老和与年龄相关的疾病.

研究的目的:

在DP条件下研究与SIRT3相关的衰老和hPDLSCs骨质分化的机制.
探索SIRT3作为PD的潜在治疗点.

主要方法:

通过高葡萄糖和脂多糖 (LPS) 刺激的hPDLSCs中检查了SIRT3表达.
评估SIRT3抑制对hPDLSC衰老和骨质分化在体外和体外的作用.
研究了SIRT3和LRPPRC之间的相互作用,以及其在氧化酸化和压力中的作用.
在DP的小鼠模型中评估了Honokiol (SIRT3激活剂) 的治疗潜力.

主要成果:

在DP相关刺激下,SIRT3表达在hPDLSCs中显著降低.
减少SIRT3加速hPDLSC衰老和骨质分化受损.
SIRT3直接去乙LRPPRC,通过氧化酸化和压力调节衰老.
在DP小鼠中,Honokiol治疗延迟了衰老和增强了膜骨再生.

结论:

激活SIRT3通过脱乙LRPPRC来抑制hPDLSC的衰老.
SIRT3-LRPPRC通路是DP中衰老和骨质分化的关键调节者.
SIRT3代表了治疗糖尿病相关牙周炎的有前途的治疗标.

关键词:

脱乙化脱乙化脱乙化霍诺基奥尔 (Honokiol) 是一个对于LRPPRCRC来说,这是一个很大的问题.牙周病是指牙周病的发生.在SIRT3中,SIRT3是最重要的.衰老是一种衰老.

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