Network pharmacology and molecular docking approach to predict the oral and topical therapeutic mechanisms of Panax ginseng ’s active compounds on atopic dermatitis

Atopic dermatitis (AD) is a recurrent inflammatory skin condition marked by itching, inflammation, and lichenification, primarily affecting children. Panax ginseng shows therapeutic promise in treating AD, although research on its mechanisms remains limited. For the first time, a network pharmacology approach was used to explore the pharmacological mechanisms of Panax ginseng's active compounds in AD treatment. Screening for bioactive compounds and their respective targets was conducted through the Traditional Chinese Medicine Systems Pharmacology (TCMSP) and SwissTargetPrediction databases. AD-related targets were gathered from GeneCards, DisGeNET, and OMIM databases. The VENNY tool was used to identify overlapping targets. STRING 12.0 was utilized for protein-protein interaction (PPI) network analysis, Cytoscape for network construction, DAVID for Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment, and PyRx AutoDock Vina for molecular docking. We retrieved 14 bioactive compounds (oral bioavailability ≥ 30% and drug-likeness ≥ 0.18) from Panax ginseng, corresponding to 552 targets, and 44 compounds (OB < 30% and DL ≥ 0.18) with 610 potential targets for oral and topical AD therapies. In the compound-target network, Gomisin B, Kaempferol, Celabenzine, and Panaxadiol emerged as key oral compounds targeting hub genes. Ginsenoside-Rh3, 12-O-nicotinoylisolineolone, Ginsenoside-Rh4, and Panaxatriol were linked to hub genes, suggesting topical application potential. GO and KEGG enrichment showed involvement of Th17 cell differentiation, EGFR tyrosine kinase inhibitor resistance, C-type lectin receptor signaling, and TNF signaling. Molecular docking showed strong binding between key compounds and core targets. This study highlights Panax ginseng's potential in complementary AD treatment.