OBJECTIVE: To probe into the potential mechanism of Ginkgo biloba in the treatment of cerebral infarction（CI） based on the method of network pharmacology. METHODS: Through the Traditional Chinese Medicine System Pharmacology Database and Analysis Platform

the highly active chemical components of Ginkgo biloba were screened and the potential targets were predicted; the CI-related targets were retrieved by GeneCards

OMIM

DisGeNET

Therapeutic Targets Database and Drugbank database. The potential targets of active ingredients of Ginkgo biloba were converted by Uniprot database and intersected with CI-related targets to obtain the relevant targets of Ginkgo biloba for the treatment of CI. The protein-protein interaction network map was constructed to screen the core genes by using STRING 11.0 database

the gene ontology function enrichment analysis and Kyoto gene and genomic encyclopedia pathway enrichment analysis were performed on the active targets of Ginkgo biloba for the treatment of CI by using Metascape software

and finally the molecular docking verification was performed with the help of software such as Auto Dock Tools. RESULTS: Totally 10 active chemical components

122 active component targets and 1 109 CI-related targets of Ginkgo biloba were detected; 43 potential targets of Ginkgo biloba for the treatment of CI were obtained after the intersection. The core active ingredients including β-sitosterol

sesamin

stigmasterol

bis[（2 S）-2-ethylhexyl] benzene-1

2-dicarboxylate

isopimelanocycline and cgenkwanin were mainly act on the core target of prostaglandin endoperoxide synthase 2（PTGS2）

and treated CI through calcium signaling pathway

adrenergic signaling pathway in toxoplasmosis and cardiac myocytes

phosphatidylinositol-3-kinase/protein kinase B（PI3 K-Akt） signaling pathway

with the main function of improving blood circulation. Results of molecular docking showed that the core active ingredients could bind well to the core targets. CONCLUSIONS: Ginkgo biloba may act on PTGS2 and other related targets through β-sitosterol

stigmasterol and sesamin

participate in inflammation

oxidation and apoptosis through the calcium signaling

PI3 K-Akt signaling and other pathways

thus exerting the pharmacological effects of multi-component

multi-target and multi-pathway in the treatment of CI.