ArticleJournal of inflammation research2025
Mechanism Exploration of Dunyeguanxinning in the Treatment of Atherosclerosis Based on UPLC-Q-Orbitrap HRMS Technology, Network Pharmacology, Molecular Docking and Experimental Validation.
Article in Journal of inflammation research, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Background: Dunyeguanxinning (DYGXN) has been shown to have therapeutic effects in preventing and treating atherosclerosis. However, the active components and anti- atherosclerosis (AS) mechanisms of DYGXN remain to be elucidated. Purpose: This study aims to explore the functional mechanisms of Dunyeguanxinning (DYGXN) in the prevention and treatment of atherosclerosis (AS). Methods: The components of DYGXN were identified using UPLC-Q-Orbitrap HRMS technology. Network pharmacology and molecular docking were utilized to explore the functional mechanisms and core targets of DYGXN. An AS mouse model was established to verify the results obtained from network pharmacology. Results: A total of 20 compounds were identified or tentatively characterized in the DYGXN solution. In total, 149 potential targets of DYGXN and 4,071 AS-related targets were obtained, with 92 overlapping targets between DYGXN and AS. The protein-protein interaction (PPI) network analysis identified 10 key targets, including SRC and STAT3, along with four core subnetworks. Gene ontology (GO) and Kyoto encyclopedia of genes and genomes (KEGG) enrichment analysis indicated that these targets were primarily involved in processes such as phosphorylation, positive regulation of cell migration, inflammatory response and pathways such as lipid and atherosclerosis. Molecular docking demonstrated strong binding affinities between DYGXN compounds and core targets. In vivo experiments showed that DYGXN improved blood lipid levels, reduced pro-inflammatory cytokines, downregulated phosphorylation of Src and STAT3, alleviated hepatic lipid accumulation, and inhibited plaque formation in AS model mice. Conclusion: DYGXN contains multiple saponins that exert anti-AS effects through the regulation of multiple targets and pathways.
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