ArticleJournal of inflammation research2025
The Effects and Mechanisms of Patchouli Alcohol on Experimental Periodontitis Rats Based on the OPG/RANK/RANKL/P38 MAPK Signaling Pathway.
Article in Journal of inflammation research, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
2 citing papers in PubMed.
- Insights into taurine therapy for periodontitis: Targeting osteocyte ferroptosis to mitigate obesity-exacerbated bone damage.Redox biology · 2026Article
- Bioceramic bone tissue-engineered substitutes with anti-inflammatory effects in periodontitis.Frontiers in bioengineering and biotechnology · 2026Review
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Authors and funding
12 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
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 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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