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This study combined systems pharmacology and computational biology to systematically investigate the multi-target mechanisms and network features of Astilbin, a natural flavonoid glycoside, in Alzheimer's disease (AD) intervention. We collected potential targets of astilbin and AD-associated genes from PharmGKB, GeneCards, and OMIM databases and screened their intersecting targets. A PPI network was built via STRING, and hub genes were screened by topological analysis in Cytoscape. GO and KEGG enrichment analyses were performed, followed by molecular docking to assess binding affinity between Astilbin and core targets. In total, 250 overlapping targets were identified. Enrichment showed these targets participate in hormone/lipid responses, carboxylic acid metabolism and kinase activities. KEGG revealed Astilbin acts via PI3K-Akt, MAPK and lipid metabolism pathways. Molecular docking verified that Astilbin exhibits low binding energy toward the core targets of Alzheimer's disease, implying a possible role in modulating neural signaling and ameliorating AD-related pathological processes. Collectively, Astilbin may contribute to AD intervention through a multi-target, multi-pathway network involving neural signaling, metabolism, inflammation, and cerebrovascular protection. This study clarifies the pharmacological mechanism of Astilbin and provides theoretical support for the development of natural product-based therapeutic agents for neurodegenerative diseases.
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Huang et al. (2026) studied this question.
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