ArticleJournal of medicinal food2014
Sulforaphane inhibits TNF-α-induced adhesion molecule expression through the Rho A/ROCK/NF-κB signaling pathway.
Article in Journal of medicinal food, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers, 1 of them a synthesis that pooled it.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
28 citing papers in PubMed, 1 synthesis or guideline pooled it, 50 citations in OpenAlex.
- Efficacy and safety of sulforaphane in schizophrenia: a systematic review and meta-analysis of randomized controlled trials.BMC psychiatry · 2025Pooled it
- A Presurgical-Window Intervention Trial of Isothiocyanate-Rich Broccoli Sprout Extract in Patients with Breast Cancer.Molecular nutrition & food research · 2022Trial
- Sulforaphane in Cutaneous Disorders and Skin Injury: Mechanisms, Evidence, and Clinical Perspectives.Nutrients · 2026Review
- Bioactive Compounds from Cruciferous Vegetables as a Therapeutic Option for the Prevention and Treatment of Cardiovascular Diseases.Nutrients · 2026Review
- Platelet-Released Growth Factors (PRGFs) Activate NRF2-ARE and Modulate Inflammatory Response in an NRF2-Dependent Manner in Primary Human Keratinocytes.Journal of cosmetic dermatology · 2025Article
- Glucosinolates in Human Health: Metabolic Pathways, Bioavailability, and Potential in Chronic Disease Prevention.Foods (Basel, Switzerland) · 2025Review
- Protective role of sulforaphane in lipid metabolism-related diseases.Molecular biology reports · 2025Review
- Protective Effects of Sulforaphane Preventing Inflammation and Oxidative Stress to Enhance Metabolic Health: A Narrative Review.Nutrients · 2025Review
- The therapeutic effects of natural organosulfur compounds on atherosclerosis and their potential mechanisms: a comprehensive review.Frontiers in cardiovascular medicine · 2025Review
- Review
- The Role of Mesenchymal Stem Cell Secretome in the Inflammatory Mediators and the Survival Rate of Rat Model of Sepsis.Biomedicines · 2023Article
- Anti-inflammatory therapy of atherosclerosis: focusing on IKKβ.Journal of inflammation (London, England) · 2023Review
- Machine learning-based identification of CYBB and FCAR as potential neutrophil extracellular trap-related treatment targets in sepsis.Frontiers in immunology · 2023Article
- Beneficial Health Effects of Glucosinolates-Derived Isothiocyanates on Cardiovascular and Neurodegenerative Diseases.Molecules (Basel, Switzerland) · 2022Review
- Epi-Drugs in Heart Failure.Frontiers in cardiovascular medicine · 2022Review
- Tumor necrosis factor-α gene promoter -308 and -238 polymorphisms and its serum level in psoriasis.Biochemistry and biophysics reports · 2021Article
- Leveraging clinical epigenetics in heart failure with preserved ejection fraction: a call for individualized therapies.European heart journal · 2021Review
- Cell-specific epigenetic changes in atherosclerosis.Clinical science (London, England : 1979) · 2021Review
- Effect of interleukin-6, -17, -21, -22, and -23 and STAT3 on signal transduction pathways and their inhibition in autoimmune arthritis.Immunologic research · 2021Review
- The Anti-Inflammatory Properties of Phytochemicals and Their Effects on Epigenetic Mechanisms Involved in TLR4/NF-κB-Mediated Inflammation.Frontiers in immunology · 2021Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Endothelial dysfunction is an early indicator of cardiovascular diseases. Increased stimulation of tumor necrosis factor-α (TNF-α) triggers the inflammatory mediator secretion of endothelial cells, leading to atherosclerotic risk. In this study, we investigated whether sulforaphane (SFN) affected the expression of intracellular adhesion molecule-1 (ICAM-1) in TNF-α-induced ECV 304 endothelial cells. Our data showed that SFN attenuated TNF-α-induced expression of ICAM-1 in ECV 304 cells. Pretreatment of ECV 304 cells with SFN inhibited dose-dependently the secretion of proinflammatory cytokines, such as interleukin (IL)-1β, IL-6, and IL-8. SFN inhibited TNF-α-induced nuclear factor-κB (NF-κB) DNA binding activity. Furthermore, SFN decreased TNF-α-mediated phosphorylation of IκB kinase (IKK) and IκBα, Rho A, ROCK, ERK1/2, and plasminogen activator inhibitor-1 (PAI-1) levels. Collectively, SFN inhibited the NF-κB DNA binding activity and downregulated the TNF-α-mediated induction of ICAM-1 in endothelial cells by inhibiting the Rho A/ROCK/NF-κB signaling pathway, suggesting the beneficial effects of SFN on suppression of inflammation within the atherosclerotic lesion.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.