ArticleNeurochemical research2023
Anticonvulsant Effects of Royal Jelly in Kainic Acid-Induced Animal Model of Temporal Lobe Epilepsy Through Antioxidant Activity.
Article in Neurochemical research, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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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.
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Who cites it
4 citing papers in PubMed, 9 citations in OpenAlex.
- Sleep and circadian rhythm disruptions in animal models of temporal lobe epilepsy.Frontiers in neuroscience · 2026Review
- Crinis Carbonisatus-Derived Carbon Dot Suspension Alleviates Temporal Lobe Epilepsy.Pharmaceuticals (Basel, Switzerland) · 2025Article
- From the different pathogenesis of epileptogenesis: vitamins as an adjunctive treatment for epilepsy.Acta epileptologica · 2025Review
- Mitochondria and oxidative stress in epilepsy: advances in antioxidant therapy.Frontiers in pharmacology · 2024Review
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Temporal lobe epilepsy (TLE) is the most common form of partial and drug-resistant epilepsy, characterized by recurrent seizures originating from temporal lobe structures like the hippocampus. Hippocampal sclerosis and oxidative stress are two important factors in the pathogenesis of TLE that exacerbate epileptic seizures in this form of epilepsy. Recently, royal jelly (RJ) shown to have neuroprotective and antioxidant activities in several neurodegenerative models. Therefore, the aim of the present study was to investigate the pretreatment effect of RJ on epileptic seizures, hippocampal neuronal loss, and oxidative stress in the rat model of kainic acid (KA)-induced TLE. To this aim, 40 male Wistar rats weighing 200-250 g were divided into 4 groups, including control, vehicle, KA, and RJ + KA. Rats received RJ (150 mg/kg/day) for 14 days before induction of TLE with KA. Epileptic behaviors were evaluated according to Racine's scale. Oxidative stress markers including, malondialdehyde (MDA), total oxidant status (TOS) and total antioxidant capacity (TAC) as well as neuronal loss in the CA1 region of the hippocampus (using Nissl staining) were evaluated in all groups. Our findings showed that RJ pretreatment significantly reduced the seizure score and increased the latency to the first seizure. RJ also reduced MDA and TOS while increasing TAC. In addition, RJ reversed neuronal damage in the hippocampal CA1 and CA3 areas. In conclusion, our results suggest that RJ has anticonvulsant and neuroprotective effects in KA induced TLE via its antioxidative properties.
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