ArticleCell death & disease2023
Sulforaphane alleviates psoriasis by enhancing antioxidant defense through KEAP1-NRF2 Pathway activation and attenuating inflammatory signaling.
Article in Cell death & disease, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 54 papers.
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Who cites it
54 citing papers in PubMed, 66 citations in OpenAlex.
- Keratinocyte-specific STAT3 knockout attenuates imiquimod-induced psoriasiform phenotype in mice.Experimental animals · 2026Article
- Circadian dysregulation of leptin and its role in skin inflammation and obesity: an integrative perspective.Endocrine · 2026Review
- LCN2-Driven Fibroblast Ferroptosis-Associated Injury Promotes Keratinocyte Proliferation via Lipid Peroxidation Signaling in Psoriasis.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026Article
- Periostin drives psoriasis progression through the stimulation of cutaneous nerve fibers.iScience · 2026Article
- Pink lotus flower (Biomedical reports · 2026Article
- TOLLIP Inhibits Psoriasis Progression via Suppressing PKM2-Mediated Glycolysis in Keratinocytes.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Nrf2 signaling pathway and its molecular regulatory mechanism.Journal of Zhejiang University. Science. B · 2026Review
- Microglial SIRT6 confers protection against neuroinflammation-associated depression through NRF2-HO1 signaling.Neurobiology of stress · 2026Article
- Characterization, Identification, and Antioxidant Mechanism of Antioxidant Peptides FromFood science & nutrition · 2026Article
- The Nox2 NADPH oxidase regulates neutrophilic inflammation in the oral cavity.Mucosal immunology · 2026Article
- Sulforaphane Alleviates Zearalenone-Induced Oxidative Stress in Bovine Mammary Epithelial Cells.Animals : an open access journal from MDPI · 2026Article
- Gut microbiota-induced perturbation in bile acids alter keratinocyte lipid metabolism via FXR-NQO1 signaling in psoriasis.Nature communications · 2026Article
- Sulforaphane in Cutaneous Disorders and Skin Injury: Mechanisms, Evidence, and Clinical Perspectives.Nutrients · 2026Review
- Article
- Plant-derived extracellular vesicles as tools and targets for inflammatory diseases.Journal of nanobiotechnology · 2026Review
- NRF2 as a Therapeutic Target in Dermatological Disorders: Mechanisms and Molecules.Pharmaceuticals (Basel, Switzerland) · 2026Review
- Study on the Antioxidant Activity of Fermented Broad Bean-Mulberry Composite Juice Based on In Vitro Digestion and Non-Targeted Metabolomic Analysis.Foods (Basel, Switzerland) · 2026Article
- Integrative bioinformatics-machine learning-experimental validation identifies shared immunomodulatory targets in psoriasis and psoriatic arthritis and deciphers allicin's therapeutic mechanism.Naunyn-Schmiedeberg's archives of pharmacology · 2026Article
- Acod1/itaconate axis controls anxiety-like behaviors induced by chronic infection of Toxoplasma gondii in mice.PLoS neglected tropical diseases · 2026Article
- Sulforaphane in Cancer Prevention and Therapy: A State-of-the-Art Review of Epidemiological Evidence, Molecular Mechanisms, and Translational Challenges.International journal of molecular sciences · 2026Review
Corrections and comments
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Authors and funding
16 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Psoriasis is a chronic inflammatory skin disease that affects millions of people worldwide. Sulforaphane (SFN) has been shown to have anti-inflammatory and antioxidant properties. In this study, we investigated the effects of SFN on a mouse model of psoriasis induced by imiquimod (IMQ) and its underlying molecular mechanism. Mice treated with SFN showed significant improvement in psoriatic symptoms, including reduced erythema, scales, and cutaneous thickness. Histopathological analysis and immunohistochemical staining revealed decreased expression of K16, K17, and Ki67 in SFN-treated mice, indicating reduced abnormal differentiation of keratinocytes and cutaneous inflammation. SFN treatment also reduced the activation of STAT3 and NF-κB pathways and downregulated pro-inflammatory cytokines IL-1β, IL-6, and CCL2. In vitro experiments using HaCaT cells demonstrated that SFN inhibited IL-22 and TNF-α-induced activation of inflammatory pathways and keratinocyte proliferation. Network pharmacology analysis suggested that the KEAP1-NRF2 pathway might be involved in the protective effects of SFN on psoriasis. We observed reduced NRF2 expression in human psoriatic lesions, and subsequent experiments showed that SFN activated KEAP1-NRF2 pathway in vivo and in vitro. Importantly, NRF2-deficient mice exhibited aggravated psoriasis-like symptoms and reduced response to SFN treatment. Our findings indicate that SFN ameliorates psoriasis symptoms and inflammation through the KEAP1-NRF2 pathway, suggesting a potential therapeutic role for SFN in the treatment of psoriasis.
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