Abstract
Carotid artery stenosis is a manifestation of atherosclerosis and is associated with an increased risk of various cardiovascular diseases. Clopidogrel is an antiplatelet drug widely used for the prevention and treatment of atherosclerosis-related diseases. This study explores the potential molecular mechanisms of clopidogrel in the treatment of carotid artery stenosis through network pharmacology and molecular docking techniques. First, network pharmacology methods were used to construct a clopidogrel target network and identify its possible 127 action targets. Secondly, the gene ontology enrichment analysis indicated that clopidogrel for treating carotid stenosis is closely related to inflammatory responses, platelet activation, and angiogenesis. The Kyoto Encyclopedia of Genes and Genomes analysis revealed associations with lipid metabolism and atherosclerosis. Subsequently, molecular docking technology was employed to screen the binding affinity of clopidogrel to these targets. The results revealed that clopidogrel exhibited binding energies less than - 4.20 kcal/mol with multiple targets, including TNF, MMP9, PTGS2, CCL2, TLR4, and IL-10. This indicates that clopidogrel has high binding affinity and stable binding modes with these targets, thereby exerting anti-inflammatory effects. This study reveals the potential molecular mechanisms of clopidogrel in the treatment of carotid artery stenosis through network pharmacology and molecular docking techniques. The experimental results provide a theoretical basis for the application of clopidogrel in the treatment of carotid artery stenosis and offer new ideas for further drug development and personalized treatment.