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已发表论文
柴胡皂苷 D 在银屑病中的潜在靶点及机制：氧化应激的生物信息学与实验研究
Authors Ding J, Sun A, Hu H, Li J, Lu S, Song J, He J, Song X, Qian S, Tian Z
Received 3 September 2025
Accepted for publication 13 November 2025
Published 26 November 2025 Volume 2025:18 Pages 16487—16507
DOI https://doi.org/10.2147/JIR.S563272
Checked for plagiarism Yes
Review by Single anonymous peer review
Peer reviewer comments 3
Editor who approved publication: Dr Anish R. Maskey
Junrui Ding,1 Aiping Sun,2 Hua Hu,1 Jialin Li,1 Shuao Lu,2 Junlan Song,2 Juao He,1 Xiangfeng Song,2 Shaoju Qian,2 Zhongwei Tian1,3
1Department of Dermatology, The First Affiliated Hospital of Xinxiang Medical University, Xinxiang, Henan, 453000, People’s Republic of China; 2School of Basic Medicine School Sciences, Xinxiang Medical University, Xinxiang, Henan, 453000, People’s Republic of China; 3General Practice School, Xinxiang Medical University, Xinxiang, Henan, 453000, People’s Republic of China
Correspondence: Zhongwei Tian, Email zhonwt@xxmu.edu.cn Shaoju Qian, Email 211032@xxmu.edu.cn
Objective: This study aims to explore the potential therapeutic effect of Saikosaponin D (SSD) on psoriasis and elucidate its underlying mechanisms, focusing on oxidative stress modulation and immune regulation.
Methods: Network pharmacology, machine learning (LASSO, SVM-RFE, Random Forest), and molecular dynamics identified Saikosaponin D’s core targets (STAT3, CCNB1) in psoriasis. Differential gene analysis (GEO datasets GSE6710, GSE50790, GSE14905), WGCNA, and PPI networks screened Saikosaponin D-psoriasis-oxidative stress intersecting genes. In vivo validation employed an imiquimod-induced psoriasis mice model with Saikosaponin D (2 mg/kg/day). Histology, qPCR, Western blot, and immune infiltration (CIBERSORT) assessed SAIKOSAPONIN D’s effects on inflammation, JAK2/STAT3 signaling, and oxidative stress markers (GPX4, SLC7A11).
Results: Saikosaponin D markedly alleviated psoriasis-like symptoms, diminishing epidermal thickness and keratinocyte proliferation, accompanied by reduced Ki67 expression. Bioinformatics investigation revealed 25 intersecting genes, with STAT3 and CCNB1 identified as principal targets. Molecular docking revealed that Saikosaponin D consistently binds to STAT3 and CCNB1, with binding energies of − 8.3 and − 9.0 kcal/mol, respectively. Saikosaponin D suppressed JAK2/STAT3 phosphorylation, leading to the downregulation of IL-1, IL-6, and TNF-α expression. Saikosaponin D enhanced GPX4 expression and reduced SLC7A11 levels, restoring oxidative equilibrium. Moreover, Saikosaponin D regulated immune infiltration by reducing M1 macrophages and augmenting Tregs, hence enhancing the psoriatic immune microenvironment.
Conclusion: Saikosaponin D suppresses psoriasis by dual-targeting STAT3/CCNB1, disrupting JAK2/STAT3 signaling and oxidative stress. This study provides new insights into the mechanism of Saikosaponin D in psoriasis, offering a promising multi-pathway therapeutic candidate.
Keywords: traditional Chinese medicine, Saikosaponin D, oxidative stress, psoriasis, network pharmacology, machine learning
1Department of Dermatology, The First Affiliated Hospital of Xinxiang Medical University, Xinxiang, Henan, 453000, People’s Republic of China; 2School of Basic Medicine School Sciences, Xinxiang Medical University, Xinxiang, Henan, 453000, People’s Republic of China; 3General Practice School, Xinxiang Medical University, Xinxiang, Henan, 453000, People’s Republic of China
Correspondence: Zhongwei Tian, Email zhonwt@xxmu.edu.cn Shaoju Qian, Email 211032@xxmu.edu.cn
Objective: This study aims to explore the potential therapeutic effect of Saikosaponin D (SSD) on psoriasis and elucidate its underlying mechanisms, focusing on oxidative stress modulation and immune regulation.
Methods: Network pharmacology, machine learning (LASSO, SVM-RFE, Random Forest), and molecular dynamics identified Saikosaponin D’s core targets (STAT3, CCNB1) in psoriasis. Differential gene analysis (GEO datasets GSE6710, GSE50790, GSE14905), WGCNA, and PPI networks screened Saikosaponin D-psoriasis-oxidative stress intersecting genes. In vivo validation employed an imiquimod-induced psoriasis mice model with Saikosaponin D (2 mg/kg/day). Histology, qPCR, Western blot, and immune infiltration (CIBERSORT) assessed SAIKOSAPONIN D’s effects on inflammation, JAK2/STAT3 signaling, and oxidative stress markers (GPX4, SLC7A11).
Results: Saikosaponin D markedly alleviated psoriasis-like symptoms, diminishing epidermal thickness and keratinocyte proliferation, accompanied by reduced Ki67 expression. Bioinformatics investigation revealed 25 intersecting genes, with STAT3 and CCNB1 identified as principal targets. Molecular docking revealed that Saikosaponin D consistently binds to STAT3 and CCNB1, with binding energies of − 8.3 and − 9.0 kcal/mol, respectively. Saikosaponin D suppressed JAK2/STAT3 phosphorylation, leading to the downregulation of IL-1, IL-6, and TNF-α expression. Saikosaponin D enhanced GPX4 expression and reduced SLC7A11 levels, restoring oxidative equilibrium. Moreover, Saikosaponin D regulated immune infiltration by reducing M1 macrophages and augmenting Tregs, hence enhancing the psoriatic immune microenvironment.
Conclusion: Saikosaponin D suppresses psoriasis by dual-targeting STAT3/CCNB1, disrupting JAK2/STAT3 signaling and oxidative stress. This study provides new insights into the mechanism of Saikosaponin D in psoriasis, offering a promising multi-pathway therapeutic candidate.
Keywords: traditional Chinese medicine, Saikosaponin D, oxidative stress, psoriasis, network pharmacology, machine learning