Exploration on Action Mechanism of Mongolian Medicine Wuwei Shaji Powder in Treating Chronic Obstructive Pulmonary Disease Based on Network Pharmacology and Molecular Docking Techniques
Abstract: Objective: To explore the potential action mechanism of Mongolian medicine Wuwei Shaji Powder (WWSJP) in treating chronic obstructive pulmonary disease (COPD) by using network pharmacology and molecular docking techniques. Methods: Potential active components and their targets of WWSJP were screened through TCMSP and SwissTargetPrediction databases. COPD-related targets were retrieved from GeneCards, OMIM, and DisGeNet databases. A Venn diagram was used to identify common targets between the medicine and the disease, and the STRING platform and Cytoscape 3.9.0 software were utilized to construct a protein-protein interaction (PPI) network and a Chinese medicine-component-target network;GO enrichment analysis and KEGG pathway enrichment analysis of the intersecting targets were performed using the DAVID database to identify key signaling pathways involved in WWSJP's treatment of COPD;core target protein structures were obtained from the PDB database,and molecular docking techniques were used to predict the binding affinity between major active components and core target proteins. Results:A total of 124 active components and 936 potential targets of WWSJP were identified,along with 816 COPDrelated targets. A total of 103 intersecting targets between the medicine and the disease were identified, mainly involving PI3K-AKT, AGE-RAGE, JAK-STAT, and MAPK signaling pathways. Molecular docking results showed that the main active components of WWSJP had strong binding abilities with VEGFA,IL-6,EGFR,PIK3CA,and JAK2,with quercetin showing the strongest binding affinity with EGFR. Conclusion:This study suggests that WWSJP can exert its therapeutic effects on COPD through multiple active components such as quercetin, kaempferol, stigmasterol, isorhamnetin, and 7-acetoxy-2-methylisoflavone. These components target VEGFA, IL-6, EGFR, PIK3CA, and JAK2, and regulate multiple signaling pathways including PI3K-AKT, AGE-RAGE, JAK-STAT, and MAPK,thereby inhibiting inflammatory reactions,oxidative stress,and apoptosis processes associated with COPD.