Objective We aimed to observe the effects of Buyang Huanwu Decoction(BYHWD) on optic tract injury of cerebral ischemia rats and to explore the effective components, core targets, and regulatory mechanism of BYHWD on cerebral ischemia rats' optic tract lesions. Methods A suture occlusion method was adopted to construct a rat model of cerebral ischemia induced by right middle cerebral artery embolization. In total, 24 male SD rats were randomly divided into the sham group, the model group, and the BYHWD group, eight rats in each group. The rats in BYHWD group were intragastrically injected with BYHWD for 30 days(16. 1 g/ kg). Optic tract damage was detected by T2 mapping, and changes in the optical tract microstructure were analyzed by diffusion tensor imaging(DTI) and diffusion tensor tractography( DTT). The active components and targets of BYHWD were collected from the TCMSP, PubMed, and CNKI databases, and the targets of ischemic optic tract injury were screened from the GeneCards, OMIM, DisGeNET, and DrugBank databases. Cytoscape was used to construct an active component- therapeutic target network. A protein-protein interaction(PPI) network was constructed, and protein cluster analysis was performed with the STRING platform. KEGG pathway analysis of core protein clusters was performed based on the Metascape database. Results T2 mapping showed that the rT2 value in the optic tract region was higher in the model group compared with the sham group(P<0. 01). The rT2 value in the optic tract region of the BYHWD group was lower compared with the model group(P<0. 01). The DTI result showed that the rFA value in the optic tract region of both the model group and the BYHWD group were lower(P<0. 01) and the rAD and rRD were higher compared with the sham group(P<0. 01). The rFA value was higher(P<0. 01) and rAD and rRD were lower (P<0. 01) in the BYHWD group compared with the model group. DTT analysis showed that the relative average length and density of nerve fibers in the optic tract region of the model group and BYHWD group were lower(P <0. 05,P <0. 01) compared with the sham group, while the relative average length and density of nerve fibers in the optic tract region of the BYHWD group were higher(P<0. 05, P<0. 01) compared with the model group. In total, 56 active components and 400 potential effective targets related to ischemic optic tract injury were screened from BYHWD. The main active components were Astragaloside IV, paeoniflorin, and ferulic acid. PPI core genes included AKT1, TNF, TP53, CASP3, and JUN. Nine related signaling pathways were obtained by KEGG pathway enrichment analysis of PPI core protein clusters. They regulate a variety of biological processes and molecular functions in neurons, astrocytes, microglia, and oligodendrocytes, mainly involving the PI3K-Akt signaling pathway, Toll-like receptor signaling pathway the apoptosis pathway, energy metabolism, and inflammatory factor-related pathways. Conclusion BYHWD can alleviate optic tract nerve injury and promote remodeling of the optic tract ultrastructure after cerebral ischemia in rats. Its effects on ischemic optic tract injury may be mediated by multiple signaling pathways, including the PI3K-Akt signaling pathway, the MAPK signaling pathway, and the TNF signaling pathway, affecting neuronal and glial cell functions. [ABSTRACT FROM AUTHOR]