05/13/2026
๐๐๐๐ก๐๐ง๐ข๐ฌ๐ฆ ๐จ๐ ๐๐๐ญ๐ข๐จ๐ง ๐จ๐ ๐๐จ๐๐๐๐ฅ๐ข๐ ๐๐ฌ๐ข๐๐ญ๐ข๐๐ (๐.) ๐๐๐ฆ. ๐ข๐ง ๐ญ๐ก๐ ๐๐ซ๐๐๐ญ๐ฆ๐๐ง๐ญ ๐จ๐ ๐๐ง๐๐จ๐ฆ๐๐ญ๐ซ๐ข๐จ๐ฌ๐ข๐ฌ ๐๐๐ฌ๐๐ ๐จ๐ง ๐๐๐ญ๐ฐ๐จ๐ซ๐ค ๐๐ก๐๐ซ๐ฆ๐๐๐จ๐ฅ๐จ๐ ๐ฒ
๐Source:Journal of Alternative Complementary & Integrative Medicine (ISSN: 2470-7562)
Background: Endometriosis (EMs) is a prevalent gynecological disorder with unclear pathogenesis, in which abnormal cell proliferation, inflammation, and immune dysregulation play central roles. Traditional Chinese medicine, including Toddalia asiatica (L.) Lam., has shown therapeutic potential, yet its mechanisms of action remain poorly elucidated.
Methods: To elucidate the mechanisms of Toddalia asiatica against EMs, a network pharmacology strategy was implemented. The active compounds, collected from TCMSP, PubChem, and published literature, underwent filtration based on SwissADME criteria. Potential targets of these compounds were identified via SwissTargetPrediction, and targets associated with EMs were retrieved from GeneCards. The interplay among compounds, targets, and the disease was visualized through a network constructed in Cytoscape. Proteinโprotein interaction networks were generated using STRING, and functional enrichment analyses (GO and KEGG) were carried out with Metascape. The binding affinities of key compounds to their targets were further validated by molecular docking simulations performed with AutoDock Vina.
Results: Our analysis identified 40 active compounds from Toddalia asiatica, with 158 corresponding targets predicted. Subsequent cross-referencing with disease databases revealed 40 of these targets were EMs-related genes. Network analysis identified ERBB2, EGFR, mTOR, AKT1, and HIF1A as central hub nodes. KEGG enrichment analysis further showed that these targets were significantly enriched in critical pathways including EGFR, PI3KโAkt, and PD-1/PD-L1 signaling. Finally, molecular docking simulations confirmed that the core compoundsโtoddacoumalone, magnoflorine, and corytuberineโexhibited strong binding affinities to the respective key targets.
Conclusion: The therapeutic effects of Toddalia asiatica against EMs are likely mediated by the modulation of cell proliferation, energy metabolism, inflammation, estrogen signaling, and the immune microenvironment, primarily through the EGFR, PI3K-Akt, and PD-1/PD-L1 pathways. Our findings provide a systematic network pharmacology foundation for its use and highlight promising targets for future experimental validation.
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