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已发表论文
基于网络药理学、实验验证和分子对接的秦皮乙素治疗银屑病的机制研究
Authors Zhang S, Du Y, Zhang H, Duan X, Li L
Received 31 May 2025
Accepted for publication 23 September 2025
Published 1 October 2025 Volume 2025:18 Pages 13535—13554
DOI https://doi.org/10.2147/JIR.S544019
Checked for plagiarism Yes
Review by Single anonymous peer review
Peer reviewer comments 2
Editor who approved publication: Dr Anish R. Maskey
Shouxu Zhang,1,2 Yue Du,1,2 Haomin Zhang,1,2 Xingwu Duan,1 Lingling Li1
1Department of Dermatology, Dongzhimen Hospital, Beijing University of Chinese Medicine, Beijing, 100700, People’s Republic of China; 2Graduate School, Beijing University of Chinese Medicine, Beijing, 100029, People’s Republic of China
Correspondence: Lingling Li, Department of Dermatology, Dongzhimen Hospital, Beijing University of Chinese Medicine, Beijing, 100700, People’s Republic of China, Email linglingli1980@163.com
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.
Keywords: psoriasis, network pharmacology, S1P, S1PR1, Th17 differentiation
1Department of Dermatology, Dongzhimen Hospital, Beijing University of Chinese Medicine, Beijing, 100700, People’s Republic of China; 2Graduate School, Beijing University of Chinese Medicine, Beijing, 100029, People’s Republic of China
Correspondence: Lingling Li, Department of Dermatology, Dongzhimen Hospital, Beijing University of Chinese Medicine, Beijing, 100700, People’s Republic of China, Email linglingli1980@163.com
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.
Keywords: psoriasis, network pharmacology, S1P, S1PR1, Th17 differentiation