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在周植入炎中,LncRNA NRIR通过通过RSAD2/NF-κB轴促进巨细胞M1极化来抑制骨质生成

Renshengjie Zhao^1,2,3, Lan Wang^1,2,3, Yang Zhou^1,2,3

¹The Affiliated Stomatological Hospital, Southwest Medical University, Luzhou, China.

Frontiers in immunology

|November 5, 2025

概括

长非编码RNANRIR通过通过RSAD2/NF-κB通路激活M1巨细胞来促进周植入炎. 减少NRIR表达抑制了炎症并增强了骨再生,提供了治疗潜力.

科学领域:

免疫学免疫学免疫学
口腔生物学口腔生物学
分子生物学分子生物学

背景情况:

牙周植入物炎涉及牙部植入物周围组织的炎症性破坏.
长非编码RNANRIR在周植入炎中被上调,并与M1巨细胞透有关.
了解NRIR在巨细胞极化中的作用对于围植入炎治疗至关重要.

研究的目的:

为了研究NRIR在围植入炎期间巨细胞两极分化中的调节作用.
阐明涉及NRIR/RSAD2/NF-κB轴的潜在分子机制.
评估在周植入炎中准NRIR的治疗潜力.

主要方法:

在使用siRNA的M1巨细胞中,NRIR和RSAD2被抑制.
通过RT-qPCR,西斑,流细胞计和免疫光测试来评估巨细胞极化和炎症标志物.
评估了NRIR调节的巨细胞对BMSC骨质分化和体内周植入炎模型的影响.

主要成果:

NRIR 倒置降低了 RSAD2 表达,并抑制了 NF-κB 途径,减少了 M1 巨细胞标记物和炎症性细胞因子.
NRIR的淘汰促进了骨髓中酶干细胞 (BMSCs) 的骨质基因分化.
在体内,NRIR knockdown-derived巨细胞超级生物降低了炎症和骨质损失,同时增强了骨质生成.

结论:

通过通过RSAD2/NF-κB轴激活M1巨细胞,NRIR作为周植入炎的促炎因素.
针对NRIR途径提供了一个潜在的策略来管理周植入炎.
这项研究为围部植入炎的病变产生提供了新的见解.

关键词:

在LncRNA NRIRIR中.在 NF-κBB 中.在RSAD2中,使用RSAD2.巨细胞的两极分化骨质性分化的骨质性差异化周植入体炎 (Peri-implantitis) 是一种疾病,

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