ZHU Junxuan, ZHANG Dong, AN Ming, XU Nanbing, FANG Longlong, WU Guodong
Objective: To explore the mechanism of Caowu-Hezi in the treatment of rheumatoid arthritis (RA) by network pharmacology and molecular docking technology. Methods: Traditional Chinese Medicine Systems Pharmacology Database and Analysis Platform (TCMSP) and literature were used to screen the effective components of Caowu-Hezi. The potential targets of the effective components were screened by Swiss Target Prediction and other databases. Based on authoritative databases such as OMIM, RA-related potential target data sets were screened. Venny online tool was used for target intersection analysis, and the screening results were imported into Cytoscape 3.7.2 software to construct protein-protein interaction networks (PPI). Gene ontology (GO) functional annotation and Kyoto encyclopedia of genes and genomics (KEGG) pathway enrichment analysis of key targets were performed through the online analysis platform. Finally, Autodock Tools molecular docking software was used to verify the molecular docking of key target proteins and potential active compounds. Results: A total of 16 active components were identified and 109 potential targets related to RA were screened out. Among them, the key targets were signal transduction and transcriptional activator protein 3 (1,STAT3), Toll-like receptor 4 (2,TLR4), transcription factor JUN, interleukin-6 (3,IL-6) and serine protein kinase (4,AKT1). Bioinformatics analysis showed that Toll-like receptor signaling pathway, tumor necrosis factor (5,TNF) signaling pathway and PI3K-Akt signaling pathway might be involved in the regulation of the pathological process of RA. Molecular docking experiments confirmed that the active components of Caowu-Hezi had high binding affinity with the above core targets (such as STAT3, TLR4, JUN, etc.), suggesting its potential regulatory role. Conclusion: Caowu-Hezi may affect the activity of target proteins such as AKT1, JUN, IL-6, STAT3 and TLR4 by regulating key signaling pathways such as Toll-like receptor, TNF and PI3K-Akt, thus exerting anti-RA effect.
