ArticleCellular and molecular life sciences : CMLS2022
Sulforaphane prevents and reverses allergic airways disease in mice via anti-inflammatory, antioxidant, and epigenetic mechanisms.
Article in Cellular and molecular life sciences : CMLS, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers, 1 of them a synthesis that pooled it.
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The trial behind it
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Who cites it
9 citing papers in PubMed, 1 synthesis or guideline pooled it, 15 citations in OpenAlex.
- Dietary sulforaphane in cancer chemoprevention: epigenetic regulation and PRMT5-MEP50 complex inhibition-a systematic review.Frontiers in pharmacology · 2026Pooled it
- From allergens to epigenetics: how histone acetylation shapes immune gene expression in allergic diseases.Epigenomics · 2025Review
- The role of Keap1-Nrf2 signaling pathway in the treatment of respiratory diseases and the research progress on targeted drugs.Heliyon · 2024Review
- Anti-Inflammatory Therapeutic Mechanisms of Isothiocyanates: Insights from Sulforaphane.Biomedicines · 2024Review
- SFX-01 in hospitalised patients with community-acquired pneumonia during the COVID-19 pandemic: a double-blind, randomised, placebo-controlled trial.ERJ open research · 2024Article
- Facile Preparation of Magnetic COF-on-COF for Rapid Adsorption and Determination of Sulforaphane from Cruciferous Vegetables.Foods (Basel, Switzerland) · 2024Article
- Bioaccessible Organosulfur Compounds in Broccoli Stalks Modulate the Inflammatory Mediators Involved in Inflammatory Bowel Disease.International journal of molecular sciences · 2024Article
- Modulation of the Immune Response to Allergies Using Alternative Functional Foods.International journal of molecular sciences · 2023Review
- Advances in respiratory physiology in mouse models of experimental asthma.Frontiers in physiology · 2023Review
Corrections and comments
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Authors and funding
21 authors at 8 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Sulforaphane has been investigated in human pathologies and preclinical models of airway diseases. To provide further mechanistic insights, we explored L-sulforaphane (LSF) in the ovalbumin (OVA)-induced chronic allergic airways murine model, with key hallmarks of asthma. Histological analysis indicated that LSF prevented or reversed OVA-induced epithelial thickening, collagen deposition, goblet cell metaplasia, and inflammation. Well-known antioxidant and anti-inflammatory mechanisms contribute to the beneficial effects of LSF. Fourier transform infrared microspectroscopy revealed altered composition of macromolecules, following OVA sensitization, which were restored by LSF. RNA sequencing in human peripheral blood mononuclear cells highlighted the anti-inflammatory signature of LSF. Findings indicated that LSF may alter gene expression via an epigenetic mechanism which involves regulation of protein acetylation status. LSF resulted in histone and α-tubulin hyperacetylation in vivo, and cellular and enzymatic assays indicated decreased expression and modest histone deacetylase (HDAC) inhibition activity, in comparison with the well-known pan-HDAC inhibitor suberoylanilide hydroxamic acid (SAHA). Molecular modeling confirmed interaction of LSF and LSF metabolites with the catalytic domain of metal-dependent HDAC enzymes. More generally, this study confirmed known mechanisms and identified potential epigenetic pathways accounting for the protective effects and provide support for the potential clinical utility of LSF in allergic airways disease.
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