Analysis of the Mechanism of Isoflavones in the Treatment of Central Arteriosclerosis Based on Network Pharmacology

The global burden of cardiovascular diseases (CVD) is on the rise. Central arteriosclerosis, a critical pathological mechanism underlying CVD, is influenced by multiple factors. Given the limitations of current single-target pharmacological interventions, there is an urgent need to investigate multi-target therapeutic strategies. This study employs a network pharmacology approach, integrating data from the SwissTargetPrediction and GeneCards databases toidentify 37 intersection targets of isoflavones and central arteriosclerosis. Aprotein-protein interaction (PPI) network is constructed to pinpoint core targets, including SRC, CASP3, ESR1, EGFR, and STAT3. Gene Ontology (GO) andKyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analyses indicate that isoflavones modulate inflammatory responses, apoptosis, andoxidative stress by regulating the "Cytokine-cytokine receptor interaction" pathway. The multi-target synergistic effects of isoflavones emulate the activityof the estrogen receptor (ESR1), inhibiting endothelial cell apoptosis and suppressing STAT3-mediated inflammatory signal transduction, thereby enhancing vascular homeostasis. In comparison to traditional statins, the multi-target mechanism of isoflavones aligns more closely with the intricate pathological network of arteriosclerosis, offering novel insights for the development of natural therapeutics. This study elucidates the comprehensive therapeutic potential of isoflavones. Future experiments are necessary to validate the specific targets and dose-response effects to facilitate clinical applications.