{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,3]],"date-time":"2026-09-03T22:10:26Z","timestamp":1788473426599,"version":"build-2803163510"},"reference-count":44,"publisher":"Wiley","issue":"8","license":[{"start":{"date-parts":[[2024,8,21]],"date-time":"2024-08-21T00:00:00Z","timestamp":1724198400000},"content-version":"vor","delay-in-days":20,"URL":"http:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Skin Research and Technology"],"published-print":{"date-parts":[[2024,8]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:sec>\n                    <jats:title>Background<\/jats:title>\n                    <jats:p>Psoriasis is a chronic inflammatory skin disease that can cause systemic inflammation in various organs. Rutin has been suggested to fight psoriasis, but the signaling pathways by which it works need to be explored.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Materials and methods<\/jats:title>\n                    <jats:p>HaCaT cells co\u2010stimulated with interleukin (IL)\u201017, IL\u201022, tumor necrosis factor\u2010alpha (TNF\u2010\u03b1), IL\u20101\u03b1, and oncostatin M (M5) were used as an in vitro cell model of psoriasis. The proliferation and viability of HaCaT cells were determined by 5\u2010ethynyl\u20102\u2032\u2010deoxyuridine and cell counting assays. Relative mRNA levels of IL\u20106, TNF\u2010\u03b1, chemokines (CXCL1 and CXCL2), and anti\u2010microbial peptides (S100A7 and S100A8) were detected by reverse transcriptase\u2010quantitative PCR. Release of IL\u20106 and TNF\u2010\u03b1 from HaCaT cells was measured by enzyme\u2010linked immunosorbent assay. Keratin1, Keratin5, p\u2010JAK2, and p\u2010STAT3 protein levels were estimated with western blotting. Molecular docking predicted binding sites for Rutin and STAT3.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>Rutin treatment undercut M5\u2010urged viability increase and proliferation boost in HaCaT cells. Moreover, M5 stimulation mediated upregulation of IL\u20106, TNF\u2010\u03b1, CXCL1, CXCL2, S100A7, and S100A8 was partially reversed after Rutin treatment. In addition, M5 stimulation induced downregulation of Keratin1 and Keratin5 proteins as well as upregulation of p\u2010JAK2 and p\u2010STAT3 proteins were attenuated in response to Rutin treatment, manifesting that Rutin treatment inhibited M5\u2010promoted aberrant differentiation and impaired M5\u2010mediated activation of the JAK2\/STAT3 signaling in HaCaT cells. Molecular docking discovered that residues GLN326 and ASP334 in STAT3 might bind to Rutin.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusion<\/jats:title>\n                    <jats:p>Rutin treatment blocked the JAK2\/STAT3 signaling, thus attenuating psoriasis\u2010related inflammation and anomalous differentiation in keratinocytes.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1111\/srt.70011","type":"journal-article","created":{"date-parts":[[2024,8,21]],"date-time":"2024-08-21T18:53:18Z","timestamp":1724266398000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":18,"title":["Rutin alleviates psoriasis\u2010related inflammation in keratinocytes by regulating the JAK2\/STAT3 signaling"],"prefix":"10.1111","volume":"30","author":[{"given":"Panhong","family":"Wu","sequence":"first","affiliation":[{"name":"Medical Beauty Department Henan Provincial Hospital 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