ORIGINAL RESEARCH article
Front. Pharmacol.
Sec. Ethnopharmacology
This article is part of the Research TopicMulti-Omics Insights into Autoimmune Diseases and Major Chronic Non-Communicable DiseasesView all 4 articles
Licoisoflavone B Alleviates Psoriasis via SCD1-Targeted Lipid Metabolism Reprogramming and Suppression of Th17/IL-17–Mediated Inflammation
Provisionally accepted
YAO LIU1*
Vincent Kam Wai Wong1*
Jiao Liu2Manling Jiang2,3Chenxu Yang1
Xiang He3
Junyi Wang3Lei Zhang3,4Anying Xiong3Qin Ran3
Xiaolan Li3Keyue Wang3Mufan Li1Peng Song1
LIANG JIN1
Guoping Li1,3*- 1Macau University of Science and Technology, Taipa, Macao, SAR China
- 2Southwest Jiaotong University, Chengdu, China
- 3Chengdu Third People's Hospital, Chengdu, China
- 4Chongqing Medical University, Chongqing, China
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Introduction: Psoriasis is a chronic inflammatory skin disorder driven by dysregulated immune responses, Th17 cells activation, and keratinocytes hyperproliferation. Despite advances in therapies, high costs and adverse effects limit their utility. Licoisoflavone B (Lico B), bioactive flavonoid derived from licorice, exhibits anti-inflammatory and metabolic modulating properties, yet its mechanisms in psoriasis remain unexplored. Methods: We employed integrative bioinformatics, including target prediction, differential expression analysis, and weighted gene co-expression network analysis to identify psoriasis-associated hub genes linked to Lico B. Functional enrichment was analyzed via GO and KEGG pathway. Molecular docking evaluated Lico B's binding affinity to candidate target. The effects of Lico B on Stearoyl-CoA Desaturase 1 (SCD1) expression, lipid metabolism, IL-17–induced keratinocyte proliferation, and Th17 differentiation. Results: Bioinformatics revealed Lico B's targets were enriched in lipid metabolism and cell cycle pathways. SCD1 emerged as a key target, supported by strong binding affinity in docking studies. Experimentally, Lico B attenuated IL-17–induced SCD1 upregulation and lipid droplet accumulation in keratinocytes. It suppressed hyperproliferation markers (KRT17/Ki67) in cells and imiquimod-induced psoriatic mice. Furthermore, Lico B reduced Th17 differentiation and IL-17 production in murine models, demonstrating dual antiproliferative and immunomodulatory effects. Conclusion: Lico B alleviates psoriasis by targeting SCD1 to modulate lipid metabolism, inhibit keratinocyte hyperproliferation, and dampen Th17/IL-17–driven inflammation. This multimodal mechanism positions Lico B as a novel therapeutic candidate for psoriasis and related inflammatory-metabolic dermatoses.
Keywords: Licoisoflavone B, Lipidmetabolism, Psoriasis, Skin, Stearoyl-CoA desaturase 1, Traditional Chinese Medicine
Received: 26 Nov 2025; Accepted: 29 Jan 2026.
Copyright: © 2026 LIU, Wong, Liu, Jiang, Yang, He, Wang, Zhang, Xiong, Ran, Li, Wang, Li, Song, JIN and Li. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
* Correspondence:
YAO LIU
Vincent Kam Wai Wong
Guoping Li
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