Objective This study utilizes network pharmacology and molecular docking techniques to explore the role of colchicine in regulating ferroptosis for the treatment of neurological injury. Methods Colchicine targets were obtained from the PubChem and Swiss Target Prediction databases, while targets related to neurological injury were retrieved from the GeneCards, OMIM, and DisGeNET databases. Ferroptosis targets were sourced from the FerrDb database, and the Venny 2.1.0 tool was accustomed to identify the intersection of these three sets. A protein-protein interaction (PPI) network was constructed based on the STRING database, and GO and KEGG pathway enrichment analyses were conducted using Metascape. Ultimately, molecular docking analyses of colchicine with the top ten targets were performed using Autodock Vina. Results There were 401 targets for colchicine, 3 367 for neurological injury, and 1 543 for ferroptosis, with 57 intersection targets. The PPI network identified TP53, IL6, EGFR, and others as major targets. KEGG analysis indicated that colchicine regulated ferroptosis through the Wnt signaling pathway to treat neurological injury. Molecular docking results showed that colchicine bound well to multiple targets. Conclusion Colchicine may regulate related genes through the Wnt signaling pathway to treat neurological injury.