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通过调节miR-24-3p/HIF1AN通路,CircPVT1促进牙周炎的进展

Yuting Bian¹, Jingwen Yu², Yang Liu¹

¹Department of Stomatology, Second Hospital of Shijiazhuang, Shijiazhuang, Hebei, 050000, PR China.

Journal of stomatology, oral and maxillofacial surgery

|February 22, 2025

概括

循环RNA circPVT1通过影响细胞活力和分化,促进牙周炎的进展. 它通过miR-24-3p/HIF1AN轴调节NRF-2/HO-1通路,为这种常见的口腔疾病提供潜在的治疗点.

科学领域:

口腔生物学口腔生物学
分子生物学分子生物学
免疫学免疫学免疫学

背景情况:

牙周炎是一种常见的慢性炎症性口腔疾病.
循环RNAs (circRNAs) 参与牙周炎的发生.
在牙周炎中circPVT1的特定作用和机制在很大程度上是未知的.

研究的目的:

研究circPVT1在牙周炎中的作用.
为了阐明circPVT1在牙周炎中的作用的潜在分子机制.

主要方法:

从牙周炎患者和健康对照组的牙组织被用RT-qPCR分析了circPVT1表达.
使用用LPS治疗的PDLC建立了牙周炎的细胞模型.
细胞活力,亡,炎症,氧化应激和骨质分化被评估使用CCK-8,流细胞计,ELISA,ALP和阿里扎林红色染色.

主要成果:

在牙周炎组织中,CircPVT1表达显著上调.
沉默circPVT1降低了细胞活力,炎症和氧化应激,同时在LPS治疗的PDLC中促进了细胞亡和骨质细胞分化.
这些效应通过抑制miR-24-3p或过度表达HIF1AN来逆转,这表明miR-24-3p/HIF1AN轴的参与.

结论:

CircPVT1会加剧牙周炎的进展.
该机制涉及通过miR-24-3p/HIF1AN轴调节NRF-2/HO-1通路.
CircPVT1代表了牙周炎的潜在治疗点.

关键词:

这就是HIF1AN.炎症炎症是一种炎症.氧化应激是一种氧化应激.牙周病是指牙周病的发生.circPVT1 的时间.在 miR-243p.

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