Exploration of the mechanism of Danggui Buxue decoction for the treatment of gastric ulcer based on network pharmacology, molecular docking, and experiment.

Objective: To explore the mechanism of Danggui Buxue decoction (, DBD) for the treatment of gastric ulcer (GU), based on network pharmacology and in vivo experiments.

Methods: A network pharmacology strategy was used to predict the main components, candidate targets, and potential signaling pathways. Then, molecular docking was performed to further investigate the interactions and binding affinities between the main components and primary targets. Finally, a mouse model of ethanol-induced gastric ulcers was established to confirm the efficacy and potential therapeutic benefits of DBD, and candidate targets were finally identified.

Results: A total of 22 active components and 220 target genes were found to be associated with DBD. In addition, 343 GU-related target genes and 57 target genes specific to DBD treatment of GU were identified. The Gene Ontology functional enrichment analysis revealed 510 entries for biological processes, 36 entries for cell composition, and 69 entries for molecular functions. In the pathway enrichment analysis, 143 signaling pathways were identified. Additionally, the molecular docking results revealed that the main active components of DBD exhibited a strong binding capacity with key proteins, including tumor necrosis factor, AKT serine/threonine kinase 1, interleukin-6, vascular endothelial growth factor, and interleukin-1 Beta. Among these, quercetin, kaempferol, formononetin, isorhamnetin, and beta-sitosterol displayed the strongest binding affinities for these key proteins. in vivo experiments showed that DBD pretreatment effectively protected gastric mucosa, and the benefits might be attributed to the downregulation of above key proteins.

Conclusions: Based on network pharmacology analysis and in vivo experiments, we conclude that DBD leads to the protection and healing of the gastric mucosa by targeting genes and pathways, thus effectively countering the development and progression of GU.