ArticleSkin research and technology : official journal of International Society for Bioengineering and the Skin (ISBS) [and] International Society for Digital Imaging of Skin (ISDIS) [and] International Society for Skin Imaging (ISSI)2024
Rutin alleviates psoriasis-related inflammation in keratinocytes by regulating the JAK2/STAT3 signaling.
Article in Skin research and technology : official journal of International Society for Bioengineering and the Skin (ISBS) [and] International Society for Digital Imaging of Skin (ISDIS) [and] International Society for Skin Imaging (ISSI), 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed.
- Polyphenols as Multi-Target Regulators of Oxidative Stress, Mitochondrial Function, and Cell Survival Signaling in Skin Diseases.International journal of molecular sciences · 2026Review
- Rutin as a multi-target anti-inflammatory phytochemical in arthritic disorders: pharmacological mechanisms and therapeutic potential.Inflammopharmacology · 2026Review
- Pink lotus flower (Biomedical reports · 2026Article
- Research Progress and Prospects of Flavonoids in the Treatment of Diseases by Regulating Autophagy: A Narrative Review.Molecules (Basel, Switzerland) · 2026Review
- Phenolic-Rich Extracts ofPlants (Basel, Switzerland) · 2025Article
- The Therapeutic Potential ofInternational journal of molecular sciences · 2025Article
- A tryptophol-containing emulgel ameliorates imiquimod-induced mice psoriasis.Scientific reports · 2025Article
- Glycitein alleviates inflammation and apoptosis in keratinocytes via ROS-associated PI3K-Akt signalling pathway.Open life sciences · 2025Article
- Potential Targets and Mechanisms of Saikosaponin D in Psoriasis: A Bioinformatic and Experimental Study on Oxidative Stress.Journal of inflammation research · 2025Article
- Rutin alleviates psoriasis-related inflammation in keratinocytes by regulating the JAK2/STAT3 signaling.Skin research and technology : official journal of International Society for Bioengineering and the Skin (ISBS) [and] International Society for Digital Imaging of Skin (ISDIS) [and] International Society for Skin Imaging (ISSI) · 2024Article
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Authors and funding
5 authors.
Funding
Abstract
backgroundPsoriasis 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. MATERIALS AND
methodsHaCaT cells co-stimulated with interleukin (IL)-17, IL-22, tumor necrosis factor-alpha (TNF-α), IL-1α, 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-ethynyl-2'-deoxyuridine and cell counting assays. Relative mRNA levels of IL-6, TNF-α, chemokines (CXCL1 and CXCL2), and anti-microbial peptides (S100A7 and S100A8) were detected by reverse transcriptase-quantitative PCR. Release of IL-6 and TNF-α from HaCaT cells was measured by enzyme-linked immunosorbent assay. Keratin1, Keratin5, p-JAK2, and p-STAT3 protein levels were estimated with western blotting. Molecular docking predicted binding sites for Rutin and STAT3.
resultsRutin treatment undercut M5-urged viability increase and proliferation boost in HaCaT cells. Moreover, M5 stimulation mediated upregulation of IL-6, TNF-α, 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-JAK2 and p-STAT3 proteins were attenuated in response to Rutin treatment, manifesting that Rutin treatment inhibited M5-promoted aberrant differentiation and impaired M5-mediated activation of the JAK2/STAT3 signaling in HaCaT cells. Molecular docking discovered that residues GLN326 and ASP334 in STAT3 might bind to Rutin.
conclusionRutin treatment blocked the JAK2/STAT3 signaling, thus attenuating psoriasis-related inflammation and anomalous differentiation in keratinocytes.
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