Unraveling the Neuroprotective Mechanisms of Cobalamin in Ischemic Stroke: A Network Pharmacology and Molecular Docking Approach

Purpose This study aims to systematically elucidate the multi-target mechanisms of cobalamin in the treatment of ischemic stroke using network pharmacology and molecular docking techniques. Methods We screened databases to identify the targets of cobalamin and performed intersection analysis with ischemic stroke-related targets to construct a "drug-target-disease" interaction network. Gene Ontology (GO) and KEGG pathway enrichment analyses were conducted to identify key biological processes and signaling pathways. Additionally, molecular docking was employed to assess the binding affinity between cobalamin and core targets. Results A total of 95 therapeutic targets of cobalamin for ischemic stroke were identified. Based on Cytoscape and molecular docking, we selected ALB, TIMP1, PLG, FN1, AGT, SERPINE1, APOE, and SPP1, which exhibited strong binding affinity. GO analysis revealed that cobalamin primarily regulates inflammatory responses, post-translational protein modifications, complement binding, and lipoprotein particle binding. KEGG pathway analysis indicated that complement and coagulation cascades, PI3K/AKT, and other inflammation-related pathways are the major signaling pathways involved in the treatment of ischemic stroke by cobalamin. Conclusion This study is the first to elucidate the molecular mechanisms through which cobalamin exerts anti-inflammatory and neuroprotective effects via multi-target and multi-pathway actions from a computational biology perspective. These findings provide new theoretical insights for the treatment of ischemic stroke with cobalamin, though further experimental validation is required.