ArticleAmerican journal of translational research2025
Bu-Yi-Xin-Shen formula targets monocytes through PI3K-Akt/NF-κB signaling in post-percutaneous coronary intervention angina.
Article in American journal of translational 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
backgroundBu-Yi-Xin-Shen formula (BYXSF) is used for the treatment of post-percutaneous coronary intervention (PCI) angina. This study combined bioinformatics and experimental verification to investigate its mechanism of action.
methodsWe retrieved relevant target data from public databases to determine candidate therapeutic targets of BYXSF in post-PCI angina. Key targets were then determined using protein-protein interaction (PPI) network and functional enrichment assays. Molecular docking was used to identify core active ingredients, while toxicity evaluation helped assess their safety profiles. After that, single-cell RNA sequencing (scRNA-seq) uncovered critical cell types and the expression patterns of target genes. Finally,
resultsFunctional enrichment analysis indicated that phosphatidylinositol 3-kinase-AKT (PI3K-Akt) and Nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) signaling pathways were significantly enriched. Combined with the high interaction degree of genes in the PPI network, PIK3R1, PIK3CA, PIK3CB, EGFR, AKT1, and SRC were determined as key targets. Then, five active ingredients (benzoylnapelline, quercetin, liquiritigenin, sexangularetin, and deltoin) with the lowest binding energies (< -8 kcal/mol) were identified by molecular docking. These active ingredients were found to influence toxicity through processes including vascular inflammation and lipid metabolism/atherosclerosis. The scRNA-seq revealed monocytes as the core cell type mediating BYXSF's therapeutic effects, with distinct expression levels of key targets between high- and low-score groups. Finally,
conclusionPIK3R1, PIK3CA, PIK3CB, EGFR, AKT1, and SRC were key genes in the PI3K-Akt and NF-κB pathways, and monocytes were major targets of BYXSF in post-PCI angina. Animal experiments validated this mechanism, laying a foundation for the further development of BYXSF as a therapeutic agent.
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