{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,6,1]],"date-time":"2026-06-01T12:58:32Z","timestamp":1780318712146,"version":"3.54.1"},"reference-count":56,"publisher":"Frontiers Media SA","license":[{"start":{"date-parts":[[2026,2,16]],"date-time":"2026-02-16T00:00:00Z","timestamp":1771200000000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"content-domain":{"domain":["frontiersin.org"],"crossmark-restriction":true},"short-container-title":["Front. Pharmacol."],"abstract":"<jats:sec>\n                    <jats:title>Introduction<\/jats:title>\n                    <jats:p>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.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>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\u2019s binding affinity to candidate target. The effects of Lico B on Stearoyl-CoA Desaturase 1 (SCD1) expression, lipid metabolism, IL-17\u2013induced keratinocyte proliferation, and Th17 differentiation.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>Bioinformatics revealed Lico B\u2019s 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\u2013induced 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.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusion<\/jats:title>\n                    <jats:p>Lico B alleviates psoriasis by targeting SCD1 to modulate lipid metabolism, inhibit keratinocyte hyperproliferation, and dampen Th17\/IL-17\u2013driven inflammation. This multimodal mechanism positions Lico B as a novel therapeutic candidate for psoriasis and related inflammatory-metabolic dermatoses.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.3389\/fphar.2026.1754729","type":"journal-article","created":{"date-parts":[[2026,2,16]],"date-time":"2026-02-16T14:16:02Z","timestamp":1771251362000},"update-policy":"https:\/\/doi.org\/10.3389\/crossmark-policy","source":"Crossref","is-referenced-by-count":1,"title":["Licoisoflavone B alleviates psoriasis via SCD1-targeted lipid metabolism reprogramming and suppression of Th17\/IL-17\u2013mediated inflammation"],"prefix":"10.3389","volume":"17","author":[{"given":"Yao","family":"Liu","sequence":"first","affiliation":[{"name":"Dr. Neher\u2019s Biophysics Laboratory for Innovative Drug Discovery, State Key Laboratory of Mechanism and Quality of Chinese Medicine, Faculty of Chinese Medicine, Macau University of Science and Technology","place":["Macao, China"]},{"name":"Dr. Neher\u2019s Biophysics 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