Abstract： Objective： To analyze the potential mechanism of ginkgetin in preventing and treating atherosclerosis （AS） based on network pharmacology and molecular docking technology. Methods： The main drug targets of ginkgetin were screened through databases such as SwissTargetPrediction and Super-PRED. The UniProt database was used to convert corresponding target protein names into gene names. The term "atherosclerosis" was searched in databases including GeneCards，DisGeNET，and TTD to obtain AS-related targets. A Venn diagram was created using the Venny 2.1 platform to identify overlapping targets between ginkgetin and AS. Cytoscape 3.10.1 software was used to construct a "drug-target-disease" network and to perform protein-protein interaction （PPI） network analysis，Gene Ontology （GO） functional enrichment， and Kyoto Encyclopedia of Genes and Genomes （KEGG） pathway analysis. Molecular docking and visualization were conducted using the AutoDock Tools platform. Results：A total of 171 ginkgetin-related targets and 4 740 AS-related targets were obtained，with 116 overlapping targets. The PPI network revealed core targets such as heat shock protein 90 alpha family class A member 1 （HSP90AA1）， B-cell lymphoma-2（ BCL-2），hypoxia-inducible factor 1-α（ HIF1A），peroxisome proliferator-activated receptor γ（ PPARG）， and caspase-3 （CASP3）. KEGG pathway analysis indicated that the main pathways included phosphatidylinositol 3-kinase-protein kinase B （PI3K-Akt） ， advanced glycation end products and their receptors in diabetic complications （AGE-RAGE）， p53， lipid and atherosclerosis， Janus kinase-signal transducer and activator of transcription （JAK-STAT），nuclear factor-kappa B （NF-κB），and apoptosis signaling pathways. Molecular docking results showed that ginkgetin exhibited strong binding affinity with core target proteins such as HSP90AA1， BCL-2， and HIF1A. Conclusion：Ginkgetin may treat AS by acting on core targets such as HSP90AA1，BCL-2，and HIF1A and regulating signaling pathways including PI3K-Akt，AGE-RAGE，p53，and lipid and atherosclerosis.