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干白素-17通过NRF2和p-STAT3之间的相互作用抑制铁亡,缓解了埃拉斯诱导的膜骨损失

Jiaqi Bao^1,2, Zhongxiu Wang¹, Yuting Yang¹

¹Department of Periodontology, The Second Affiliated Hospital, College of Medicine, Zhejiang University, Hangzhou, China.

Journal of clinical periodontology

|November 14, 2023

概括

介质蛋白-17 (IL-17) 保护铁亡并促进牙周炎模型中的骨质分化. 这涉及p-STAT3-NRF2复合体,为骨修复提供潜在的治疗点.

科学领域:

细胞生物学细胞生物学
生物化学生物化学
牙周病学牙周病学

背景情况:

铁亡,一种受调节的细胞死亡途径,以及骨质分化在牙周组织恒温中至关重要.
介质蛋白-17 (IL-17) 在炎症性骨疾病中起作用,但其在铁亡和骨质生成中的特定参与需要阐明.

研究的目的:

在牙周炎的背景下调查IL-17,铁和骨质分化之间的相互作用.
探索 IL-17 的作用背后的分子机制,包括 NRF2 和 p-STAT3 的作用.

主要方法:

在实验性牙周炎模型中分析与铁亡相关的分子.
在体内研究评估埃拉斯和IL-17对膜骨损失和修复的影响.
在实验室实验中,用埃拉斯和IL-17治疗的小鼠骨质母细胞进行了基因/蛋白质表达分析.
通过siRNA,免疫光和免疫沉来确认NRF2和p-STAT3的作用和相互作用.

主要成果:

在牙周炎组织中,NRF2和铁灭调节剂 (GPX4,SLC7A11) 的水平降低.
埃拉斯加剧了膜骨损失,而IL-17则减轻了这种损失.
通过减轻ferroptosis在体外,IL-17逆转了埃拉斯诱导的骨质分化的抑制.
在核中确定了NRF2和p-STAT3之间的物理相互作用,形成了一个影响铁和骨质生成相关基因转录的复合体.

结论:

给予IL-17会对埃拉斯诱导的骨质细胞铁和骨质生成产生抗性.
IL-17的保护机制可能涉及骨质细胞内p-STAT3和NRF2之间的直接相互作用.

关键词:

它的IL-17是IL-17.这就是NRF2的NRF2.气泡骨损失是指气泡骨损失的发生.铁性化 (ferroptosis) 是一种骨质发生过程 (osteogenesis)

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