The interaction mechanism between active ingredients of honeysuckle and uric acid metabolism genes

Abstract

Objective: This study utilizes the integrated approach of network pharmacology combined with molecular docking to investigate the mechanism of action of honeysuckle in reducing hyperuricemia. Method: The active constituents and potential targets of honeysuckle were retrieved from the TCMSP, PubChem, SwissTargetPrediction, and UniProt databases. The hyperuricemia-associated targets were acquired from GeneCards and OMIM databases, and Draw Venn Diagram website was used to find common targets between the drug and the disease. Then use the STRING database to construct a PPI network of key targets and screen for core targets. GO and KEGG enrichment analyses were carried out through the David database and a component-target-pathway network was drawn using Cytoscape_v3.9.1 software. Finally, molecular docking was conducted using CB-Dock2 website and Discovery Studio software to verify the binding activity of the effective components with the core targets. Results: Upon screening, 23 active components of honeysuckle, 502 component targets, and 1375 disease targets were identified, with 125 common targets. GO and KEGG enrichment analysis results show that the active components of honeysuckle significantly participate in biological processes such as anti-inflammatory, anti-apoptotic, and gene expression regulation, involving molecular functions like enzyme binding and protein kinase activity. They also treat hyperuricemia through multiple signaling pathways, including the AGE-RAGE signaling pathway and cancer-related pathways. Molecular docking results show that the core targets IL6、TNF and TP53 have good binding activity with luteolin, quercetin, and kaempferol. Conclusion: Multiple active components in honeysuckle can synergistically treat hyperuricemia through multi-component, multi-target, and multi-pathway approaches. The potential mechanism of action may involve influencing key targets such as IL6、TNF and TP53, thereby regulating multiple pathways to exert uric acid-lowering effects.