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在炎症性环境下,牙牙带干细胞的骨质性机制

Jin-Yi Li^1,2, Shan-Shan Dai^1,2, Zheng-Yang Li^1,2

¹Key Laboratory of Shaanxi Province for Craniofacial Precision Medicine Research, College of Stomatology, Xi'an Jiaotong University, Xi'an, China.

Brazilian journal of medical and biological research = Revista brasileira de pesquisas medicas e biologicas

|October 9, 2024

概括

脂聚糖 (LPS) 影响叶牙牙带干细胞 (DePDLSCs) 双相,低度刺激,高度抑制细胞功能. 激活PI3K-AKT通路可以减轻LPS的影响,为牙周炎治疗提供了洞察力.

科学领域:

牙科干细胞生物学牙科干细胞生物学
炎症的分子机制
阿皮克牙周炎的发病因子

背景情况:

阿皮牙周炎涉及落叶牙的复杂细胞和分子变化.
叶牙牙带干细胞 (DePDLSCs) 在保持牙健康和再生方面发挥着至关重要的作用.
了解像脂多糖 (LPS) 这样的细菌成分对DePDLSCs的影响对于阐明疾病进展至关重要.

研究的目的:

调查DePDLSCs在牙周炎进展期间的生物行为和功能变化.
探索分子机制,特别是PI3K-AKT信号通路,涉及LPS诱导对DePDLSCs的影响.
评估调节PI3K-AKT通路的潜力,用于治疗牙周炎的治疗干预.

主要方法:

对DePDLSCs的隔离和表征.
使用CCK-8,实时PCR,ALP染色和LPS治疗后活动测定来评估细胞活力,炎症和骨质生成潜力.
高通量测序以确定受LPS影响的分子通路.
使用激活器 (740Y-P) 对PI3K-AKT信号通路的干扰,以评估其在调节LPS效应中的作用.

主要成果:

LPS对DePDLSCs表现出双相作用,在低度刺激增殖和骨质生成,在高度抑制它们.
高通量测序显示,在LPS暴露 (10微克/毫升) 时,PI3K-AKT信号通路的显著下调.
用740Y-P治疗部分挽救了LPS对炎症和骨质生成的抑制作用,表明该途径的参与.

结论:

LPS以度依赖的双相方式影响DePDLSC的增殖和骨质生成.
适度激活PI3K-AKT信号通路可促进骨质生分化,并对DePDLSCs产生抗炎作用.
准PI3K-AKT通路为治疗落叶牙的顶端牙周炎提供了潜在的治疗策略.

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