Objective: To explore the material basis of Ginkgo biloba extract Ginaton and its potential mechanism in the treatment of pathological scar by network pharmacology-molecular docking-experimental verification method. Methods: The key word 'Ginkgo biloba' was input into DGIdb, DrugBank, Swiss Target Prediction and TCMSP databases to obtain the target of Ginaton. The disease-related targets of pathological scar lesions were obtained from GeneCards, DisGeNET, OMIM and DrugBank databases, and the intersection of the above targets was taken as the target of Ginaton′s anti-pathological scar effect. The target was uploaded to the STRING database, and the obtained data were imported into Cytoscape 3.9.1 to construct a protein interaction network and screen out the core targets. GO and KEGG enrichment analysis was performed on the target genes of Ginaton′s disease-resistant rational scar using the DAVID database. The binding force between the core target and Ginaton was verified by molecular docking. In addition, a mouse pathological scar model was established to verify the role of Ginaton in resisting pathological scar formation. Results: A total of 38 targets of Ginaton against pathological scar were obtained, and 7 core target genes were screened, which were MAPK1, JUN, IL6, FOS, TNF, MAPK14 and AKT1, respectively. KEGG pathway analysis enriched signaling pathways including: AGE-RAGE signaling pathway in diabetic complications, lipid and atherosclerosis, IL-17 signaling pathway, etc. Molecular docking showed that the core target genes MAPK1, MAPK14 and AKT1 had good affinity with Ginaton, especially with quercetin, luteolin and kaempferol. The administration experiment of pathological scar model in mice showed that compared with the model group, the expression of TGF-β1 in pathological scar tissue of mice injected with 20 mg/(kg·d) Ginaton was significantly decreased (P＜0.05). Conclusion: Ginaton has a multi-target and multi-pathway character in anti-pathological scar generation. Ginaton primarily acts on core target genes such as MAPK1, MAPK14 and AKT1, and affects the PI3K/AKT/mTOR pathway and the MAPK signaling pathway to exert therapeutic effects on pathological scarring.
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