广藿香醇对实验性牙周炎大鼠OPG/RANK/RANKL/P38 MAPK信号通路的影响及其机制

IF 4.1 2区 医学 Q2 IMMUNOLOGY
Journal of Inflammation Research Pub Date : 2025-09-13 eCollection Date: 2025-01-01 DOI:10.2147/JIR.S530534
Shuting Zhang, Feifei Duan, Tianzhen He, Chaoqun Sun, Menglu Zhen, Enxi Liang, Xingduo Liu, Yuqiong Dai, Ruoting Zhan, Nianchun Hu, Yun Xia, Sijun Liu
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引用次数: 0

摘要

背景:广藿香在中药中长期用于治疗炎症性疾病,其主要活性成分广藿香醇(PA)也具有抗炎作用。然而,PA在牙周炎治疗中的潜在分子机制尚不清楚。研究目的:本研究的主要目的是通过OPG/RANK/RANKL/p38 MAPK信号通路观察PA对实验性牙周炎大鼠的影响。材料与方法:采用结扎联合LPS注射大鼠牙周炎模型,观察PA对牙周炎的治疗作用。利用靶点预测、靶点筛选、交叉靶点鉴定、蛋白-蛋白相互作用(PPI)网络构建和拓扑分析、基因本体(GO)和京都基因与基因组百科全书(KEGG)富集分析以及分子对接等方法预测PA的潜在药理机制。采用Micro-CT检测牙槽骨丢失,ELISA检测炎症,qRT-PCR和Western blot进一步证实其作用机制。结果:网络药理学提示p38 MAPK信号通路是PA治疗牙周炎的主要机制。PA治疗可减少牙周炎大鼠牙骨质与牙槽骨嵴之间的距离。ELISA和H&E染色结果显示,PA可减轻炎症反应,降低IL-6、TNF-α、IL-1β水平。qRT-PCR分析显示,PA显著提高了RUNX2和OPG的mRNA表达水平,降低了RANK、RANKL、NFATc1和TRAF6的mRNA表达水平。Western blot结果显示,PA显著降低RANKL、RANK和MMP9的表达,同时显著提高OPG的表达。结论:PA是治疗牙周炎的有效策略,其作用机制可能与抑制牙槽骨丢失和调节OPG/RANK/RANKL/p38 MAPK通路有关。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
The Effects and Mechanisms of Patchouli Alcohol on Experimental Periodontitis Rats Based on the OPG/RANK/RANKL/P38 MAPK Signaling Pathway.

Background: Patchouli has been used for a long time in traditional Chinese medicine to treat inflammatory diseases, and its main active component, patchouli alcohol (PA), also has anti-inflammatory effects. However, the underlying molecular mechanism of PA in the periodontitis treatment is not well understood.

Aim of the study: The primary objective of this study was to examine the effects of PA on experimental periodontitis in rats through the lens of the OPG/RANK/RANKL/p38 MAPK signaling pathway.

Materials and methods: A rat model of periodontitis induced by ligation combined with LPS injection was used to evaluate the therapeutic effects of PA on periodontitis. Target prediction, target screening, intersection target identification, protein-protein interaction (PPI) network construction and topological analysis, Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analyses, along with molecular docking were employed to predict the potential pharmacological mechanisms of PA. Micro-CT was utilized to detect alveolar bone loss, ELISA was used to measure inflammation, and qRT-PCR and Western blot were performed to further confirm its mechanisms of action.

Results: Network pharmacology indicated that the p38 MAPK signaling pathway is the primary mechanism by which PA treats periodontitis. PA treatment reduced the distance between the cementum and the alveolar bone crest in rats with periodontitis. ELISA and H&E staining results showed that PA alleviated the inflammatory response and reduced the levels of IL-6, TNF-α, and IL-1β. qRT-PCR analysis revealed that PA significantly increased the mRNA expression levels of RUNX2 and OPG, and decreased the mRNA expression levels of RANK, RANKL, NFATc1, and TRAF6. Western blot revealed that PA significantly reduced the expression of RANKL, RANK, and MMP9 while significantly elevating OPG expression.

Conclusion: PA is an effective therapeutic strategy for periodontitis, and its mechanism of action involves inhibiting alveolar bone loss and modulating the OPG/RANK/RANKL/p38 MAPK pathway.

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来源期刊
Journal of Inflammation Research
Journal of Inflammation Research Immunology and Microbiology-Immunology
CiteScore
6.10
自引率
2.20%
发文量
658
审稿时长
16 weeks
期刊介绍: An international, peer-reviewed, open access, online journal that welcomes laboratory and clinical findings on the molecular basis, cell biology and pharmacology of inflammation.
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