Network pharmacology reveals that Huayu Jiedu formula activates the PI3K/Akt pathway to mitigate acute cerebral infarction, suggesting therapeutic potential.
Huayu Jiedu formula (HYJDF), a traditional Chinese herbal compound effective against acute cerebral infarction (ACI), lacks a defined mechanism of action. HYJDF's bioactive components were identified via ultra-high-performance liquid chromatography-Quadrupole-Exactive-mass spectrometry (UHPLC-QE-MS). Network pharmacology integrated the Traditional Chinese Medicine Systems Pharmacology Database and Analysis Platform database-predicted ACI targets and multiple databases to construct herb-component-target networks (Cytoscape). Core targets were prioritized through protein-protein interaction network analysis (STRING) and topological filtering (degree/closeness/betweenness centrality). Pathway enrichment (Kyoto Encyclopedia of Genes and Genomes [KEGG] Database for Annotation, Visualization, and Integrated Discovery) and molecular docking (AutoDock Vina) were performed. Key findings were validated in vivo using a middle cerebral artery occlusion rat model. UHPLC-QE-MS identified 1041 components; 229 were ACI-relevant. Topological analysis revealed 29 core targets (e.g., TP53, STAT3, interleukin [IL]6, tumor necrosis factor [TNF], and Akt1). KEGG enrichment implicated the PI3K/Akt pathway. Molecular docking confirmed high-affinity binding between HYJDF components (e.g., arachidonic acid and baicalein) and targets (Akt1 and IL6). In vivo, HYJDF treatment upregulated PI3K/Akt phosphorylation, suppressed neuroinflammation, and attenuated cerebral ischemic injury. HYJDF mediates therapeutic effects against ACI primarily by activating the PI3K/Akt signaling pathway and downregulating associated inflammatory factors.
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Liu et al. (2025) studied this question.
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