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Peer-reviewedCC BY-NC 4.0Clinical, Cosmetic and Investigational Dermatology

Exploring the Molecular Mechanisms of Yinxieping Tablets in Psoriasis Treatment Based on Network Pharmacology, Bioinformatics, and Experimental Validation

  1. 1Department of Dermatology, Shaanxi Provincial Hospital of Chinese Medicine, Xi’an, Shaanxi, 710003, People’s Republic of China

Abstract

Introduction: Psoriasis is a prevalent immune-mediated chronic inflammatory skin disease, with a pathology defined by abnormal keratinocyte proliferation and immune cell infiltration. Yinxieping Tablets (YXPT), a traditional Chinese medicine formula consisting solely of rosin, have been clinically used to alleviate psoriatic symptoms. However, their underlying mechanisms of action remain to be fully elucidated.

Methods: We established an imiquimod (IMQ)-induced psoriasis-like mouse model and systematically screened the potential targets and pathways of YXPT using integrated network pharmacology, bioinformatics, machine learning, transcriptome sequencing, and molecular docking. Key findings were experimentally validated by Western blot and qPCR in a psoriasis-like mouse model.

Results: YXPT treatment improved psoriasiform skin lesions and was associated with lower lesional Ki67 expression and serum pro-inflammatory cytokine levels; high-dose YXPT also reduced the spleen index. Integrated analyses identified six candidate genes (BCL2, LYN, SYK, CCR2, AURKA, and ADRB2), with CCR2 emerging as the sole overlap with RNA-seq-derived genes. CCR2-based gene-set analysis showed enrichment of PI3K/Akt- and NF-κB-related pathways. Following YXPT treatment, lesional CCR2 protein and mRNA levels, phosphorylation of PI3K, Akt, p38, and p65, and mRNA levels of PI3K, Akt, p38, ERK1/2, and p65 were lower than in the IMQ group.

Conclusion: YXPT ameliorated psoriasis-like skin lesions in the IMQ mouse model, accompanied by lower CCR2 expression and changes in PI3K/Akt, MAPK, and NF-κB pathway components. These findings nominate CCR2 as a candidate for further study, while its causal role and relationship to the signaling changes remain to be established.

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BibTeX
@article{zhu2026exploring,
  title = {{Exploring the Molecular Mechanisms of Yinxieping Tablets in Psoriasis Treatment Based on Network Pharmacology, Bioinformatics, and Experimental Validation}},
  author = {Zhengjin Zhu and Ling Ma and Dan Sun and Wenbin Li and Jinfeng Zhao},
  journal = {Clinical, Cosmetic and Investigational Dermatology},
  year = {2026},
  month = oct,
  doi = {10.2147/ccid.s646149},
  url = {https://doi.org/10.2147/ccid.s646149},
  note = {CC BY-NC 4.0},
}
RIS
TY  - JOUR
TI  - Exploring the Molecular Mechanisms of Yinxieping Tablets in Psoriasis Treatment Based on Network Pharmacology, Bioinformatics, and Experimental Validation
AU  - Zhengjin Zhu
AU  - Ling Ma
AU  - Dan Sun
AU  - Wenbin Li
AU  - Jinfeng Zhao
PY  - 2026
DA  - 2026/10/30
JO  - Clinical, Cosmetic and Investigational Dermatology
DO  - 10.2147/ccid.s646149
UR  - https://doi.org/10.2147/ccid.s646149
AB  - Introduction: Psoriasis is a prevalent immune-mediated chronic inflammatory skin disease, with a pathology defined by abnormal keratinocyte proliferation and immune cell infiltration. Yinxieping Tablets (YXPT), a traditional Chinese medicine formula consisting solely of rosin, have been clinically used to alleviate psoriatic symptoms. However, their underlying mechanisms of action remain to be fully elucidated.  Methods: We established an imiquimod (IMQ)-induced psoriasis-like mouse model and systematically screened the potential targets and pathways of YXPT using integrated network pharmacology, bioinformatics, machine learning, transcriptome sequencing, and molecular docking. Key findings were experimentally validated by Western blot and qPCR in a psoriasis-like mouse model.  Results: YXPT treatment improved psoriasiform skin lesions and was associated with lower lesional Ki67 expression and serum pro-inflammatory cytokine levels; high-dose YXPT also reduced the spleen index. Integrated analyses identified six candidate genes (BCL2, LYN, SYK, CCR2, AURKA, and ADRB2), with CCR2 emerging as the sole overlap with RNA-seq-derived genes. CCR2-based gene-set analysis showed enrichment of PI3K/Akt- and NF-κB-related pathways. Following YXPT treatment, lesional CCR2 protein and mRNA levels, phosphorylation of PI3K, Akt, p38, and p65, and mRNA levels of PI3K, Akt, p38, ERK1/2, and p65 were lower than in the IMQ group.  Conclusion: YXPT ameliorated psoriasis-like skin lesions in the IMQ mouse model, accompanied by lower CCR2 expression and changes in PI3K/Akt, MAPK, and NF-κB pathway components. These findings nominate CCR2 as a candidate for further study, while its causal role and relationship to the signaling changes remain to be established.
SN  - 1178-7015
ER  -