Objective: To investigate the possible molecular mechanism of panax notoginseng in the treatment of vitreous hemorrhage (VH). Methods: The active components of Panax notoginseng were screened by TCMSP database and the corresponding targets were collected. Vh-related gene targets were derived from GeneCards and OMIM database, and the target of Panax notoginseng was mapped to disease target genes. STRING database and Cytoscape 3.7.2 software were used to construct the protein-protein interaction (PPI) network diagram and the interaction network of "Pantoginseng - active ingredient - VH-target protein", and the core action target genes were screened out. Finally, gene body (GO) biological process and metabolic pathway enrichment analysis of KEGG were performed on the potential therapeutic targets. Results: We identified 8 active components, 162 active component targets, 1387 VH-related genes and 75 candidate targets for VH. In the "Panax notoginseng - active ingredient-VH-target protein" interaction network, there are 82 nodes in total. The core target genes include AKT1, CASP3, VEGF-A, IL-6 and MMP-9. 143 major enrichment pathways were identified by GO and KEGG enrichment analysis. The key signal pathways include age-RAGE signaling pathway, fluid shear stress and atherosclerosis, etc., and the significant molecular functions include cytokine activity, receptor ligand activity, cytokine receptor binding, etc. Conclusion: The potential molecular mechanism of panax notoquinone in the treatment of VH is closely related to the biological processes of anti-angiogenesis, anti-inflammation, regulation of apoptosis and oxidative stress, and AKT1, CASP3, VEGF-A, IL-6 and MMP-9 may be the core target genes.