Mechanistic Insights into Qin Bi Yin for Psoriasis Treatment Using Network Pharmacology, Experimental Validation, and Molecular Docking.

OBJECTIVE

In this study, we investigated the potential mechanism of action of Qing Bi Yin (QBY) in psoriasis treatment via regulation of the sphingosine-1-phosphate (S1P)/sphingosine-1-phosphate receptor 1 (S1PR1) pathway and Th17 cell differentiation.

METHODS

Network pharmacology was used to identify potential targets and elucidate the potential mechanisms of QBY in psoriasis. The predicted mechanisms were validated with in vitro Th17 cell differentiation assays using isolated mouse splenic CD4+ T cells. Molecular docking was performed to evaluate the binding affinities between active compounds and key target proteins.

RESULTS

We identified 262 overlapping QBY psoriasis target genes. Kyoto Encyclopedia of Genes and Genomes (KEGG) analysis showed significant associations with the sphingolipid signaling pathway, Th17 cell differentiation, and IL-17 signaling pathway. Network algorithms were used to identify 10 key active compounds and five hub genes. QBY treatment suppresses S1P synthesis and S1pr1 expression in Th17-polarized cells. QBY inhibited Th17 cell proliferation and differentiation, reduced inflammatory cytokine secretion by Th17 cells via the S1P/S1PR1 pathway, and modulated STAT3 and SMAD2 phosphorylation. Molecular docking showed strong binding affinities between active compounds (glabridin, luteolin, licoflavone A, and isobutyrylshikonin) from QBY and key targets (STAT3, SMAD2, SPHK1, and RORγt) in Th17 cells.

CONCLUSION

QBY ameliorates psoriatic inflammation by regulating Th17 cell differentiation via the S1P/S1PR1 signaling pathway. These findings underscore the clinical translational potential of QBY and its active constituent glabridin.