ArticleTranslational neuroscience2019
Nox2-dependent Neuroinflammation in An EAE Model of Multiple Sclerosis.
Article in Translational neuroscience, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed, 39 citations in OpenAlex.
- Redox Imbalance in CD4+ T Cells of Relapsing-Remitting Multiple Sclerosis Patients.Oxidative medicine and cellular longevity · 2020Trial
- NADPH oxidases: redox regulation of cell homeostasis and disease.Physiological reviews · 2025Review
- Design of Benzyl-triazolopyrimidine-Based NADPH Oxidase Inhibitors Leads to the Discovery of a Potent Dual Covalent NOX2/MAOB Inhibitor.Journal of medicinal chemistry · 2025Article
- Panobinostat Attenuates Experimental Autoimmune Encephalomyelitis in Mice via Suppressing Oxidative Stress-Related Neuroinflammation and Mitochondrial Dysfunction.International journal of molecular sciences · 2024Article
- Oxidative Stress Markers in Multiple Sclerosis.International journal of molecular sciences · 2024Review
- Pathological high intraocular pressure induces glial cell reactive proliferation contributing to neuroinflammation of the blood-retinal barrier via the NOX2/ET-1 axis-controlled ERK1/2 pathway.Journal of neuroinflammation · 2024Article
- NOX-induced oxidative stress is a primary trigger of major neurodegenerative disorders.Progress in neurobiology · 2023Review
- Roles and regulation of microglia activity in multiple sclerosis: insights from animal models.Nature reviews. Neuroscience · 2023Review
- Article
- Identification of significant modules and hub genes involved in hepatic encephalopathy using WGCNA.European journal of medical research · 2022Article
- Risk Factors from Pregnancy to Adulthood in Multiple Sclerosis Outcome.International journal of molecular sciences · 2022Review
- Impact of CYBA genotypes on severity and progression of multiple sclerosis.European journal of neurology · 2022Article
- Chronic experimental autoimmune encephalomyelitis is an excellent model to study neuroaxonal degeneration in multiple sclerosis.Frontiers in molecular neuroscience · 2022Review
- Inhibition of lysophosphatidic acid receptor 1-3 deteriorates experimental autoimmune encephalomyelitis by inducing oxidative stress.Journal of neuroinflammation · 2021Article
- ROS Live Cell Imaging During Neuronal Development.Journal of visualized experiments : JoVE · 2021Article
- Microglial Nox2 Plays a Key Role in the Pathogenesis of Experimental Autoimmune Encephalomyelitis.Frontiers in immunology · 2021Article
- Comparison of Thalamus and Basal Ganglia Signs Between Multiple Sclerosis and Primary Angiitis of the Central Nervous System: An Exploratory Study.Frontiers in neurology · 2021Article
- Interleukin-4-Mediated Oxidative Stress Is Harmful to Hippocampal Neurons of Prothrombin Kringle-2-Lesioned Rat In Vivo.Antioxidants (Basel, Switzerland) · 2020Article
- Review
- Dysregulation of metabolic pathways by carnitine palmitoyl-transferase 1 plays a key role in central nervous system disorders: experimental evidence based on animal models.Scientific reports · 2020Article
Corrections and comments
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Authors and funding
9 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundMultiple sclerosis (MS) is an inflammatory disease of the CNS, characterized by demyelination, focal inflammatory infiltrates and axonal damage. Oxidative stress has been linked to MS pathology. Previous studies have suggested the involvement of NADPH oxidase 2 (Nox2), an enzyme that catalyzes the reduction of oxygen to produce reactive oxygen species, in the MS pathogenesis. The mechanisms of Nox2 activation on MS are unknown. The purpose of this study was to investigate the effect of Nox2 deletion on experimental autoimmune encephalomyelitis (EAE) onset and severity, on astrocyte activation as well as on pro-inflammatory and anti-inflammatory cytokine induction in striatum and motor cortex. METHODOLOGY: Subcutaneous injection of MOG35-55 emulsified with complete Freund's adjuvant was used to evaluate the effect of Nox2 depletion on EAE-induced encephalopathy. Striatum and motor cortices were isolated and evaluated by immunoblotting and RT-PCR.
resultsNox2 deletion resulted in clinical improvement of the disease and prevented astrocyte activation following EAE induction. Nox2 deletion prevented EAE-induced induction of pro-inflammatory cytokines and stimulated the expression of the anti-inflammatory cytokines IL-4 and IL-10.
conclusionsOur data suggest that Nox2 is involved on the EAE pathogenesis. IL-4 and IL-10 are likely to be involved on the protective mechanism observed following Nox2 deletion.
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