The mechanism of Croci stigma in the treatment of melasma based on network pharmacology and molecular docking.

Purpose: To investigate the molecular mechanism of Croci stigma (CS) in the treatment of melasma by network pharmacology and molecular docking.

Methods: TCMSP, CTD, STITCH, SymMap, GeneCard, GenBank, OMIM and DrugBank databases were used to obtain the components and targets of CS and the targets of chloasma. STRING was used to build a protein-protein interaction (PPI) network of intersecting targets between drugs and diseases. Cytoscape was used to establish drug-compounds-targets-disease network and analyze PPI network. R was used for Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analysis and visualization. AutoDock was used for molecular docking and R was used to visualize docking results.

Results: Four active compounds were screened out from CS, and 31 target genes intersecting with melasma were found after further analysis. The top 10 hub genes were found after analysis of the PPI network, including TYR, TYRP1, DCT, CREB1, KITLG, MITF, ESR1, EDNRB, CD4, and PTGS2. In the enrichment analysis, melanogenesis was considered as the core pathway through which CS exerts its therapeutic effect on melasma. Molecular docking results showed that the core genes in the regulatory network had high binding activity with related active components, especially crocetin.

Conclusion: CS may treat melasma by regulating core targets, such as TYR, TYRP1, DCT, CREB1, KITLG, MITF, EDNRB, and PTGS2, and acting on melanogenesis. And crocetin may be the core compound worthy of further study.