ArticleExperimental and therapeutic medicine2020
Antiepileptic effects of exogenous β-hydroxybutyrate on kainic acid-induced epilepsy.
Article in Experimental and therapeutic medicine, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT05674552 (Efficacy of Exogenous Ketone Esters for Children With Refractory Convulsive Status Epileptics), which is not on this map. Cited by 3 papers.
What it found
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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.
Efficacy of Exogenous Ketone Esters for Children With Refractory Convulsive Status Epileptics
Who cites it
3 citing papers in PubMed, 9 citations in OpenAlex.
- Analysis of the efficacy and safety of inpatient and outpatient initiation of KD for the treatment of pediatric refractory epilepsy using generalized estimating equations.Frontiers in neurology · 2023Article
- Beta-Hydroxybutyrate: A Dual Function Molecular and Immunological Barrier Function Regulator.Frontiers in immunology · 2022Review
- Ketone Bodies in the Brain Beyond Fuel Metabolism: From Excitability to Gene Expression and Cell Signaling.Frontiers in molecular neuroscience · 2021Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The aim of the present study was to explore the potential anticonvulsant effects of β-hydroxybutyrate (BHB) in a kainic acid (KA)-induced rat epilepsy model. The KA-induced rat seizure model was established and BHB was administrated intraperitoneally at a dose of 4 mmol/kg 30 min prior to KA injection. Hippocampal tissues were then obtained 1, 3 and 7 days following KA administration, following which the expression levels of neuron-specific enolase (NSE) and glial fibrillary acidic protein (GFAP) were measured using a double immunofluorescence labeling method. In addition, the contents of glutathione (GSH), γ-aminobutyric acid (GABA) and ATP were measured using ELISA. Pretreatment with BHB markedly increased the expression of NSE after KA injection compared with that in the normal saline (NS) + KA group, suggesting that the application of BHB could alleviate neuronal damage in rats. The protective effect of BHB may be associated with suppressed inflammatory responses, which was indicated by the observed inhibition of GFAP expression in rats in the BHB + KA group compared with that in the NS + KA group. It was also found that GSH and GABA contents were notably increased after the rats were pretreated with BHB compared with those in the NS + KA group. To conclude, the application of exogenous BHB can serve as a novel therapeutic agent for 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 OpenQuestion graph.