Network Pharmacology and Molecular Docking on the Mechanism of Epimedium in the Treatment of Chronic Obstructive Pulmonary Disease
Chunyu Pan, Yusheng Wang, Yue Li, Zixuan He, Hao Chen, Zhou Li, Hui Fu, Shuze Zhuang, Jianqiang LiuIntroduction:
To investigate the mechanism of Epimedium in the treatment of Chronic Obstructive Pulmonary Disease (COPD) using network pharmacology and molecular docking approaches.
Methods:
The active components and corresponding targets of Epimedium were screened from the Traditional Chinese Medicine Systems Pharmacology (TCMSP) database. COPD-related disease targets were obtained from the OMIM and GeneCards databases. All target genes were standardized using the UniProt database. Protein-Protein Interaction (PPI) networks, Gene Ontology (GO) enrichment, and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analyses were performed using the ClusterProfiler R package and the STRING database. The herb-compound-target network and the target-pathway network were constructed in Cytoscape to identify core compounds, key targets, and major pathways. Finally, molecular docking between the core targets and the active compounds was performed using AutoDock Vina.
Results:
A total of 23 active components and 223 corresponding targets of Epimedium were identified in the treatment of COPD. The core targets included TP53, IL1B, AKT1, TNF, and IL6. GO enrichment analysis indicated that biological processes were primarily enriched in responses to lipopolysaccharide, molecules of bacterial origin, epithelial cell proliferation and injury repair, and regulation of apoptotic signaling pathways. KEGG pathway enrichment yielded 200 signaling pathways; after excluding irrelevant pathways, the most significantly enriched pathways were predominantly associated with inflammation and immune regulation, including the PI3KAkt, TNF, IL-17, AGE-RAGE, and p53 signaling pathways. Molecular docking results demonstrated that the active compounds of Epimedium exhibited favorable binding affinities with IL-1β, IL-6, and TNF.
Discussion:
These findings suggest that Epimedium exerts therapeutic effects against COPD through a multicomponent, multi-target, and multi-pathway regulatory mechanism. The integrated network pharmacology and molecular docking analyses indicate that modulation of inflammatory and oxidative stress-related pathways may represent the principal molecular basis underlying its pharmacological activity, providing mechanistic support for future experimental validation.
Conclusion:
Epimedium exhibits the multi-component, multi-target, and multi-pathway characteristics of traditional Chinese medicine. Its therapeutic effects in COPD are mediated through active ingredients such as quercetin, kaempferol, and luteolin, which regulate core targets including IL-1β, IL-6, TNF, and TP53, and modulate inflammation- and immune-related pathways such as PI3K-Akt, AGE-RAGE, and IL-17. These actions collectively contribute to anti-inflammatory and anti-oxidative stress effects, regulation of pulmonary apoptosis, and inhibition of pulmonary vascular and airway remodeling. This study tried to apply network pharmacology and molecular docking to elucidate the multi-target synergistic mechanism of Epimedium in the treatment of COPD, providing a theoretical basis for subsequent experimental validation and drug development.