Experimental study reveals patchouli alcohol reduces inflammation and alveolar bone loss in periodontitis, demonstrating its role in modulating the OPG/RANK/RANKL pathway.
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. 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. 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. 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. 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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Zhang et al. (2025) studied this question.
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