ArticleJournal of neuroinflammation2018
NADPH oxidases as potential pharmacological targets against increased seizure susceptibility after systemic inflammation.
Article in Journal of neuroinflammation, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
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Who cites it
29 citing papers in PubMed, 55 citations in OpenAlex.
- Effect of high altitude on the pharmacokinetics and pharmacodynamics of valproate in epileptic rats.Frontiers in pharmacology · 2026Article
- Inhibition of NOX4-Mediated ROS Production Contributes to Selenomethionine's Anti-Inflammatory Effect in LPS-Stimulated Bovine Endometrial Epithelial Cells.Veterinary sciences · 2025Article
- On the utility of immobilized phenylarsine oxide in the study of redox sensitive cardiac proteins.Scientific reports · 2025Article
- Anti-epileptic and Neuroprotective Effects of Ultra-low Dose NADPH Oxidase Inhibitor Dextromethorphan on Kainic Acid-induced Chronic Temporal Lobe Epilepsy in Rats.Neuroscience bulletin · 2024Article
- Diet-derived circulating antioxidants and risk of epilepsy: a Mendelian randomization study.Frontiers in neurology · 2024Article
- The emerging role of oxidative stress in inflammatory bowel disease.Frontiers in endocrinology · 2024Review
- Suppression by central adenosine A3 receptors of the cholinergic defense against cardiovascular aberrations of sepsis: role of PI3K/MAPKs/NFκB signaling.Frontiers in pharmacology · 2024Article
- Stimulation of the Pro-Resolving Receptor Fpr2 Reverses Inflammatory Microglial Activity by Suppressing NFκB Activity.International journal of molecular sciences · 2023Article
- Daytime-Restricted Feeding Ameliorates Oxidative Stress by Increasing NRF2 Transcriptional Factor in the Rat Hippocampus in the Pilocarpine-Induced Acute Seizure Model.Brain sciences · 2023Article
- Complement C3 Enhances LPS-Elicited Neuroinflammation and Neurodegeneration Via the Mac1/NOX2 Pathway.Molecular neurobiology · 2023Article
- Association of patent foramen ovale with epilepsy: A hospital-based case-control study.Epilepsia open · 2023Article
- Dysfunction of NRG1/ErbB4 Signaling in the Hippocampus Might Mediate Long-term Memory Decline After Systemic Inflammation.Molecular neurobiology · 2023Article
- Therapeutic Strategies to Ameliorate Neuronal Damage in Epilepsy by Regulating Oxidative Stress, Mitochondrial Dysfunction, and Neuroinflammation.Brain sciences · 2023Review
- Chronic stress but not acute stress decreases the seizure threshold in PTZ-induced seizure in mice: role of inflammatory response and oxidative stress.Naunyn-Schmiedeberg's archives of pharmacology · 2023Article
- Specific inhibition of NADPH oxidase 2 modifies chronic epilepsy.Redox biology · 2022Article
- Endoplasmic reticulum stress and unfolded protein accumulation correlate to seizure recurrence in focal cortical dysplasia patients.Cell stress & chaperones · 2022Article
- Relationship between chronic hypoxia and seizure susceptibility.CNS neuroscience & therapeutics · 2022Review
- Conditional knockout of ASK1 in microglia/macrophages attenuates epileptic seizures and long-term neurobehavioural comorbidities by modulating the inflammatory responses of microglia/macrophages.Journal of neuroinflammation · 2022Article
- Hydroxysafflor Yellow A Blocks HIF-1Antioxidants (Basel, Switzerland) · 2022Article
- TNFα-mediated necroptosis in brain endothelial cells as a potential mechanism of increased seizure susceptibility in mice following systemic inflammation.Journal of neuroinflammation · 2022Article
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 1 country.
Funding
Abstract
backgroundSystemic inflammation associated with sepsis can induce neuronal hyperexcitability, leading to enhanced seizure predisposition and occurrence. Brain microglia are rapidly activated in response to systemic inflammation and, in this activated state, release multiple cytokines and signaling factors that amplify the inflammatory response and increase neuronal excitability. NADPH oxidase (NOX) enzymes promote microglial activation through the generation of reactive oxygen species (ROS), such as superoxide anion. We hypothesized that NOX isoforms, particularly NOX2, are potential targets for prevention of sepsis-associated seizures.
methodsTo reduce NADPH oxidase 2-derived ROS production, mice with deficits of NOX regulatory subunit/NOX2 organizer p47
resultsIncreased susceptibility to PTZ-induced seizures following sepsis was significantly attenuated in gp91
conclusionsOur results indicate that NADPH oxidases contribute to the development of increased seizure susceptibility in mice after sepsis. Pharmacologic inhibition of NOX may be a promising therapeutic approach to reducing sepsis-associated neuroinflammation, neuronal hyperexcitability, and seizures.
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