Background: Panax notoginseng, a Chinese herbal medicine, has been widely used to
treat vascular diseases. Diabetic retinopathy (DR) is one of the complications of diabetic
microangiopathy. According to recent studies, the application of Panax notoginseng extract and
related Chinese patent medicine preparations can significantly improve DR. However, the
pharmacological mechanisms remain unclear. Therefore, the purpose of this study was to decipher
the potential mechanism of Panax notoginseng treatment of DR using network pharmacology.
Methods: We evaluated and screened the active compounds of Panax notoginseng using the
Traditional Chinese Medicine Systems Pharmacology database and collected potential targets of
the compounds by target fishing. A multi-source database was also used to organize targets of DR.
A potential target as a treatment of DR with Panax notoginseng was then obtained by matching the
compound targets with the DR targets. Using protein-protein interaction networks and topological
analysis, interactions between potential targets were identified. In addition, we also performed
gene ontology-biological process and pathway enrichment analysis using the Kyoto Encyclopedia
of Genes and Genomes.
Results: Eight active ingredients of Panax notoginseng and 31 potential targets for the treatment of
DR were identified. The screening and enrichment analysis revealed that the treatment of DR using
Panax notoginseng primarily involved 28 biological processes and 10 related pathways. Further
analyses indicated that angiogenesis, inflammatory reactions, and apoptosis may be the main
processes involved in the treatment of DR with Panax notoginseng. In addition, we determined that
the mechanism of intervention of Panax notoginseng in treating DR may involve five core targets,
VEGFA, MMP-9, MMP-2, FGF2, and COX-2.
Conclusion: Panax notoginseng may treat diabetic retinopathy through the mechanism of network
pharmacological analysis. The underlying molecular mechanisms were closely related to the
intervention of angiogenesis, inflammation, and apoptosis with VEGFA, MMP-9, MMP-2, FGF2,
and COX-2 being possible targets.