ArticleNeurochemical research2013
Antioxidant, anticonvulsive and neuroprotective effects of dapsone and phenobarbital against kainic acid-induced damage in rats.
Article in Neurochemical research, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 31 citations in OpenAlex.
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- Ursolic acid derivative UA312 ameliorates ionizing radiation-induced cardiotoxicity and neurodevelopmental toxicity in zebrafish via targeting chrna3 and grik5.Acta pharmacologica Sinica · 2025Article
- The antifibrotic effect of Vildagliptin and Diaminodiphenyl Sulfone in murine schistosomiasis mansoni.Scientific reports · 2025Article
- Dapsone improves the vincristine-induced neuropathic nociception by modulating neuroinflammation and oxidative stress.Daru : journal of Faculty of Pharmacy, Tehran University of Medical Sciences · 2022Article
- A comprehensive insight into the anti-inflammatory properties of dapsone.Naunyn-Schmiedeberg's archives of pharmacology · 2022Review
- Dapsone, More than an Effective Neuro and Cytoprotective Drug.Current neuropharmacology · 2022Review
- Combination of antiseizure medications phenobarbital, ketamine, and midazolam reduces soman-induced epileptogenesis and brain pathology in rats.Epilepsia open · 2021Article
- Clozapine Induced Developmental and Cardiac Toxicity on Zebrafish Embryos by Elevating Oxidative Stress.Cardiovascular toxicology · 2021Article
- Research Supporting a Pilot Study of Metronomic Dapsone during Glioblastoma Chemoirradiation.Medical sciences (Basel, Switzerland) · 2021Article
- Inhibition of TRIB3 Protects Against Neurotoxic Injury Induced by Kainic Acid in Rats.Frontiers in pharmacology · 2019Article
- Gastrodin Suppresses Pentylenetetrazole-Induced Seizures Progression by Modulating Oxidative Stress in Zebrafish.Neurochemical research · 2018Article
- Neuroprotection as a Potential Therapeutic Perspective in Neurodegenerative Diseases: Focus on Antiepileptic Drugs.Neurochemical research · 2016Review
- Anti-Apoptotic Effects of Dapsone After Spinal Cord Injury in Rats.Neurochemical research · 2015Article
- Recovery of Dementia Syndrome following Treatment of Brain Inflammation.Dementia and geriatric cognitive disorders extraArticle
- Validating a model of benzodiazepine refractory nerve agent-induced status epilepticus by evaluating the anticonvulsant and neuroprotective effects of scopolamine, memantine, and phenobarbital.Journal of pharmacological and toxicological methodsArticle
- Protective Effects of Dapsone on Scopolamine-Induced Memory Impairment in Mice: Involvement of Nitric Oxide Pathway.Dementia and geriatric cognitive disorders extraArticle
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Excitotoxicity due to glutamate receptors (GluRs) overactivation is a leading mechanism of oxidative damage and neuronal death in various diseases. We have shown that dapsone (DDS) was able to reduce both neurotoxicity and seizures associated to the administration of kainic acid (KA), an agonist acting on AMPA/KA receptors (GluK1-GluK5). Recently, it has been shown that phenobarbital (PB) is also able to reduce epileptic activity evoked by that receptor. In the present study, we tested the antioxidative, anticonvulsive and neuroprotective effects of DDS and PB administered alone or in combination upon KA toxicity to rats. Results showed that KA increased lipid peroxidation and diminished reduced glutathione (GSH), 24 h after KA administration and both drugs in combination or individually inhibited these events. Likewise, KA promotes mortality and this event was antagonized by effect of both treatments. Additionally, the behavioral evaluation showed that DDS and PB administered alone or in combination decreased the number of limbic seizures and reduced the percentage of animals showing tonic-clonic seizures versus the control group, which was administered only with KA. Finally, our study demonstrated that all of the treatments prevented the neuronal death of the pyramidal cell layer of hippocampal CA-3. In conclusion, the treatment with DDS and PB administrated alone or in combination exerted antioxidant, anticonvulsive and neuroprotective effects against the neurotoxicity induced by KA in rats, but their effects were not additive. Thus, it may be good options of treatment in diseases such as epilepsy and status epilepicus, administered separately.
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