ArticleScientific reports2015
Resveratrol Treatment after Status Epilepticus Restrains Neurodegeneration and Abnormal Neurogenesis with Suppression of Oxidative Stress and Inflammation.
Article in Scientific reports, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 papers, 1 of them a synthesis that pooled it.
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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.
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Who cites it
48 citing papers in PubMed, 1 synthesis or guideline pooled it, 86 citations in OpenAlex.
- Dose-related Effects of Resveratrol in Different Models of Pulmonary Arterial Hypertension: A Systematic Review.Current cardiology reviews · 2020Pooled it
- Healing from the Ocean: Targeting Shared Mechanisms in Autism and Epilepsy Using Algae-Derived Compounds.Marine drugs · 2026Review
- Ethnopharmacological relevance of Chinese medicinal materials and natural products in epilepsy: a critical multi-target review integrating neurons, glia and inflammatory signaling.Frontiers in pharmacology · 2026Review
- MTH1 in the disorders of the central nervous system: scope beyond brain tumors and challenges.Acta neurologica Belgica · 2025Review
- Pathophysiology of Status Epilepticus Revisited.International journal of molecular sciences · 2025Review
- Residual microglia following short-term PLX5622 treatment in 5xFAD mice exhibit diminished NLRP3 inflammasome and mTOR signaling, and enhanced autophagy.Aging cell · 2025Article
- Role of Plant Phytochemicals: Resveratrol, Curcumin, Luteolin and Quercetin in Demyelination, Neurodegeneration, and Epilepsy.Antioxidants (Basel, Switzerland) · 2024Review
- Oral antioxidant edaravone protects against cognitive deficits induced by chronic hypobaric hypoxia at high altitudes.Translational psychiatry · 2024Article
- NCBP1 Improves Cognitive Function in Mice by Reducing Oxidative Stress, Neuronal Loss, and Glial Activation After Status Epilepticus.Molecular neurobiology · 2023Article
- Complications of COVID-19 on the Central Nervous System: Mechanisms and Potential Treatment for Easing Long COVID.Aging and disease · 2023Review
- Therapeutic Strategies to Ameliorate Neuronal Damage in Epilepsy by Regulating Oxidative Stress, Mitochondrial Dysfunction, and Neuroinflammation.Brain sciences · 2023Review
- An aqueous extract ofHeliyon · 2022Article
- Resveratrol Prevents Cytoarchitectural and Interneuronal Alterations in the Valproic Acid Rat Model of Autism.International journal of molecular sciences · 2022Article
- Oral Nano-Curcumin in a Model of Chronic Gulf War Illness Alleviates Brain Dysfunction with Modulation of Oxidative Stress, Mitochondrial Function, Neuroinflammation, Neurogenesis, and Gene Expression.Aging and disease · 2022Article
- Pharmacological Effects ofPharmaceuticals (Basel, Switzerland) · 2022Article
- Pharmacological modulation of cytokines correlating neuroinflammatory cascades in epileptogenesis.Molecular biology reports · 2022Review
- Cannabis sativa and/or melatonin do not alter brain lipid but alter oxidative mechanisms in female rats.Journal of cannabis research · 2021Article
- Epilepsy Associated Depression: An Update on Current Scenario, Suggested Mechanisms, and Opportunities.Neurochemical research · 2021Review
- Role of Modulation of Hippocampal Glucose Following Pilocarpine-Induced Status Epilepticus.Molecular neurobiology · 2021Article
- Micronized Resveratrol Shows Anticonvulsant Properties in Pentylenetetrazole-Induced Seizure Model in Adult Zebrafish.Neurochemical research · 2021Article
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
Abstract
Antiepileptic drug therapy, though beneficial for restraining seizures, cannot thwart status epilepticus (SE) induced neurodegeneration or down-stream detrimental changes. We investigated the efficacy of resveratrol (RESV) for preventing SE-induced neurodegeneration, abnormal neurogenesis, oxidative stress and inflammation in the hippocampus. We induced SE in young rats and treated with either vehicle or RESV, commencing an hour after SE induction and continuing every hour for three-hours on SE day and twice daily thereafter for 3 days. Seizures were terminated in both groups two-hours after SE with a diazepam injection. In contrast to the vehicle-treated group, the hippocampus of animals receiving RESV during and after SE presented no loss of glutamatergic neurons in hippocampal cell layers, diminished loss of inhibitory interneurons expressing parvalbumin, somatostatin and neuropeptide Y in the dentate gyrus, reduced aberrant neurogenesis with preservation of reelin + interneurons, lowered concentration of oxidative stress byproduct malondialdehyde and pro-inflammatory cytokine tumor necrosis factor-alpha, normalized expression of oxidative stress responsive genes and diminished numbers of activated microglia. Thus, 4 days of RESV treatment after SE is efficacious for thwarting glutamatergic neuron degeneration, alleviating interneuron loss and abnormal neurogenesis, and suppressing oxidative stress and inflammation. These results have implications for restraining SE-induced chronic temporal lobe epilepsy.
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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 Socratic graph.