ArticleMolecular neurobiology2023
Protective Effect of Sulforaphane on Oxidative Stress and Mitochondrial Dysfunction Associated with Status Epilepticus in Immature Rats.
Article in Molecular neurobiology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers, 1 of them a synthesis that pooled it.
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Who cites it
17 citing papers in PubMed, 1 synthesis or guideline pooled it, 26 citations in OpenAlex.
- Efficacy and safety of sulforaphane in schizophrenia: a systematic review and meta-analysis of randomized controlled trials.BMC psychiatry · 2025Pooled it
- Anxiolytic and Anticonvulsant Effects ofBiology · 2026Article
- Sulforaphane mitigates behavioral deficits in experimental chronic kidney disease through regulation of Nrf2/NLRP3 inflammasome.Naunyn-Schmiedeberg's archives of pharmacology · 2026Article
- In Vivo Longitudinal Mapping of Brain Iron Accumulation After Pilocarpine-Induced Status Epilepticus.Molecular neurobiology · 2026Article
- Canine Idiopathic Epilepsy as a Natural Animal Model for Human Epilepsy: A Scoping Review Highlighting Metabolic Perspectives Beyond the Brain.Nutrients · 2026Article
- From clinical practice to mechanistic insights in ketogenic diets for epilepsy.The Lancet. Neurology · 2026Review
- Transcriptomic analysis revealed the protective role of genistein against oxidized fish oil-induced oxidative stress and inflammatory responses in turbot (Frontiers in physiology · 2026Article
- The Redox Revolution in Brain Medicine: Targeting Oxidative Stress with AI, Multi-Omics and Mitochondrial Therapies for the Precision Eradication of Neurodegeneration.International journal of molecular sciences · 2025Review
- Glucosinolate Metabolites and Brain Health: An Updated Review on Their Potential Benefits in Neurodegenerative, Neurodevelopmental, and Psychiatric Disorders.Antioxidants (Basel, Switzerland) · 2025Review
- Sulforaphane and Brain Health: From Pathways of Action to Effects on Specific Disorders.Nutrients · 2025Review
- VDAC1 Inhibition Mitigates Inflammatory Status and Oxidative Stress in Epileptic Mice Treated with the Ketogenic Diet.Neurochemical research · 2025Article
- Plant Secondary Metabolites as Modulators of Mitochondrial Health: An Overview of Their Anti-Oxidant, Anti-Apoptotic, and Mitophagic Mechanisms.International journal of molecular sciences · 2025Review
- Broccoli for the brain: a review of the neuroprotective mechanisms of sulforaphane.Frontiers in cellular neuroscience · 2025Review
- Kidney Injury in a Murine Hemorrhagic Shock/Resuscitation Model Is Alleviated by sulforaphane's Anti-Inflammatory and Antioxidant Action.Inflammation · 2024Article
- Nrf2 as a potential target for the treatment of epilepsy.Neural regeneration research · 2024Article
- Epilepsy Research in the Institute of Physiology of the Czech Academy of Sciences in Prague.Physiological research · 2024Review
- Sulforaphane Ameliorates High-Fat-Diet-Induced Metabolic Abnormalities in Young and Middle-Aged Obese Male Mice.Foods (Basel, Switzerland) · 2024Article
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
The present study aimed to elucidate the effect of sulforaphane (a natural isothiocyanate) on oxidative stress and mitochondrial dysfunction during and at selected periods following status epilepticus (SE) induced in immature 12-day-old rats by Li-pilocarpine. Dihydroethidium was employed for the detection of superoxide anions, immunoblot analyses for 3-nitrotyrosine (3-NT) and 4-hydroxynonenal (4-HNE) levels and respiratory chain complex I activity for evaluation of mitochondrial function. Sulforaphane was given i.p. in two doses (5 mg/kg each), at PD 10 and PD 11, respectively. The findings of the present study indicate that both the acute phase of SE and the early period of epileptogenesis (1 week and 3 weeks following SE induction) are associated with oxidative stress (documented by the enhanced superoxide anion production and the increased levels of 3-NT and 4-HNE) and the persisting deficiency of complex I activity. Pretreatment with sulforaphane either completely prevented or significantly reduced markers of both oxidative stress and mitochondrial dysfunction. Since sulforaphane had no direct anti-seizure effect, the findings suggest that the ability of sulforaphane to activate Nrf2 is most likely responsible for the observed protective effect. Nrf2-ARE signaling pathway can be considered a promising target for novel therapies of epilepsy, particularly when new compounds, possessing inhibitory activity against protein-protein interaction between Nrf2 and its repressor protein Keap1, with less "off-target" effects and, importantly, with an optimal permeability and bioavailability properties, become available commercially.
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Registered trials
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