Background: Recurrent aphthous ulcers significantly impact patients' quality of life due to their painful and recurrent nature, necessitating more effective treatments. This study explores the therapeutic potential of Boswellia to treat recurrent aphthous ulcers by its anti-inflammatory and healing promotion effect in a rat oral ulcer model.
Methods: Network pharmacology techniques were employed to elucidate Boswellia's active components and potential targets. Intersecting targets of Boswellia and oral ulcer-related genes were screened for protein-protein interaction network analysis and functional enrichment. An oral ulcer model in rats was used and rats were treated with Boswellia extract. The healing process was monitored by measuring the ulcer area and body weight changes. Histological analysis was performed, and the role of Boswellia in macrophage polarization was investigated through gene expression analysis and protein array tests. The underlying mechanism involving PPARγ activation was also explored.
Results: Network pharmacology analysis revealed Boswellia's interaction with key genes and pathways associated with inflammation and lipid metabolism, such as MAPK3, PPARG, and PTGS2. Boswellia extract significantly accelerated oral ulcer healing and recovered weight loss in rats. Histological examinations revealed reduced tissue swelling and inflammatory cell infiltration in treated groups. Furthermore, Boswellia extract decreased infiltration of M1 macrophage presence while increasing M2 macrophage, indicating an inflammation-resolving effect. In vitro studies showed that Boswellia extract enhanced M2-related gene expression and decreased pro-inflammatory cytokines, which is PPARγ dependent.
Conclusion: Boswellia extract promotes oral ulcer healing and resolves inflammation, primarily through the modulation of macrophage polarization via PPARγ activation.
Keywords: Boswellia; PPARγ; inflammation; macrophage; oral Ulcers.
© 2025 John Wiley & Sons A/S. Published by John Wiley & Sons Ltd.