Abstract: Objective This study aims to explore the effects of Perillaldehyde (PAH) on genes associated with Cerebral ischemic injury(CII) using network pharmacology and molecular docking. Methods The physicochemical properties and targets of PAH were identified through network pharmacology platforms such as PubChem, TCMSP, PharmMapper and UniProt. Disease targets associated with CII were retrieved from Gene cards, DisGenet and OMIM disease databases. The intersection targets of PAH and CII were visualized using a Venn diagram. A Protein-Protein Interaction (PPI) network was constructed using the STRING platform, and key targets along with their related pathways were screened using Cytoscape software and enrichment analysis. Finally, Molecular docking was used to predicted the key molecules of the interaction between PAH and CII. Results Network pharmacology analysis identified a total of 790 non-redundant potential targets of PAH from the PharmMapper, Swisstargetprediction, and Target-Net platforms. Concurrently, a total of 4250 unique targets of CII were retrieved from the Gene cards,DisGenet and OMIM platforms. A Venn diagram identified 373 intersection targets PAH and CII. PPI and Cytoscape analysis yielded 186 key targets. Enrichment analysis revealed that PAH and CII were mainly associated with processes including metabolism, postsynaptic membrane potential, intercellular adhesion,apoptosis, T-cell selection, cytoskeleton organization, calcium ion transport, and telencephalic cell migration. Molecular docking revealed that core targets for the successful docking between PAH and CII include Akt1, Bcl 2 and Gsk3b of CII. Conclusions PAH ameliorates CII by regulating core targets Akt1, Bcl 2 and Gsk3b, thereby influencing processes such as metabolism, apoptosis and cell migration.