ArticleClinics (Sao Paulo, Brazil)2024
Keap1/Nrf2 signaling pathway participating in the progression of epilepsy via regulation of oxidative stress and ferroptosis in neurons.
Article in Clinics (Sao Paulo, Brazil), 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed.
- In Vivo Longitudinal Mapping of Brain Iron Accumulation After Pilocarpine-Induced Status Epilepticus.Molecular neurobiology · 2026Article
- Anti-Inflammatory and Antioxidant Strategies in Epilepsy: From Molecular Mechanisms to Threshold Management.International journal of molecular sciences · 2026Review
- SAT1 Knockdown Decreases Glutamate-Induced Oxidative Stress, Ferroptosis, and Apoptosis in HT22 Cells via Activating the Nrf2/ARE Pathway.Neuromolecular medicine · 2025Article
- Discovery of placental microRNAs associated with maternal insulin sensitivity during pregnancy.Placenta · 2025Article
- Integrated immune, hormonal, and transcriptomic profiling reveals sex-specific dysregulation in long COVID patients with ME/CFS.Cell reports. Medicine · 2025Article
- Ketogenic Diet and Neuroinflammation: Implications for Neuroimmunometabolism and Therapeutic Approaches to Refractory Epilepsy.Nutrients · 2024Review
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Authors and funding
6 authors.
Funding
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Abstract
objectiveThis study aims to analyze the relationship between the Kelch-like ECH-associated protein 1 (Keap1)/Nuclear factor-erythroid 2-related factor 2 (Nrf2) and Epilepsy (EP), as well as its mechanism of action.
methodsThirty Wistar rats were divided into a control group (without treatment), a model group (EP modeling), and an inhibition group (EP modeling + intervention by Keap1/Nrf2 signaling pathway inhibitor ATRA) and subject to Morris water maze experiment. Then, the expression of Oxidative Stress (OS) markers, ferroptosis-associated proteins and Keap1/Nrf2 pathway in rat hippocampus was measured. In addition, rat hippocampal neuronal cell HT22 was purchased and treated accordingly based on the results of grouping, and cell proliferation and apoptosis in the three groups were determined.
resultsCompared with rats in the model group, those in the inhibition group showed shorter escape latency and an increased number of platform crossings (p < 0.05). Significant OS and neuron ferroptosis, increased apoptosis rate, elevated Keap1 expression, and decreased Nrf2 expression were observed in the model group compared to the control group (p < 0.05). The inhibition group exhibited notably improved OS and ferroptosis, as well as enhanced neuronal viability (p < 0.05).
conclusionInhibition of the Keap1/Nrf2 pathway can reverse the OS and neuron viability in EP rats.
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