ArticleJournal of neuroinflammation2015
Inhibition of NADPH oxidase activation reduces EAE-induced white matter damage in mice.
Article in Journal of neuroinflammation, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers.
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Who cites it
45 citing papers in PubMed, 74 citations in OpenAlex.
- Tracking CNS and systemic sources of oxidative stress during the course of chronic neuroinflammation.Acta neuropathologica · 2015Trial
- Chronic granulomatous disease: lessons in cell biology from monogenic immunodeficiency.Clinical and experimental immunology · 2025Review
- Autophagy-mediated regulation of neutrophil inflammatory responses and its relevance to central nervous system diseases.Frontiers in aging neuroscience · 2025Review
- Antioxidant Therapies in the Treatment of Multiple Sclerosis.Biomolecules · 2024Review
- Metabolic Control of Microglia.Advances in neurobiology · 2024Review
- NOX-induced oxidative stress is a primary trigger of major neurodegenerative disorders.Progress in neurobiology · 2023Review
- Neuroprotective Effects of Sinomenine on Experimental Autoimmune Encephalomyelitis via Anti-Inflammatory and Nrf2-Dependent Anti-Oxidative Stress Activity.Neuromolecular medicine · 2023Article
- Neutrophils in Inflammatory Diseases: Unraveling the Impact of Their Derived Molecules and Heterogeneity.Cells · 2023Review
- Zinc and Central Nervous System Disorders.Nutrients · 2023Review
- β-Adrenoceptor Blockade Moderates Neuroinflammation in Male and Female EAE Rats and Abrogates Sexual Dimorphisms in the Major Neuroinflammatory Pathways by Being More Efficient in Males.Cellular and molecular neurobiology · 2023Article
- EROS is a selective chaperone regulating the phagocyte NADPH oxidase and purinergic signalling.eLife · 2022Article
- Ultrafine Diesel Exhaust Particles Induce Apoptosis of Oligodendrocytes by Increasing Intracellular Reactive Oxygen Species through NADPH Oxidase Activation.Antioxidants (Basel, Switzerland) · 2022Article
- 2,3,5,4'-Tetrahydroxystilbene-2-O-β-glucoside Attenuates Reactive Oxygen Species-Dependent Inflammation and Apoptosis inAntioxidants (Basel, Switzerland) · 2022Article
- NADPH Oxidase: a Possible Therapeutic Target for Cognitive Impairment in Experimental Cerebral Malaria.Molecular neurobiology · 2022Article
- Edaravone Inhibits the Production of Reactive Oxygen Species in Phagocytosis- and PKC-Stimulated Granulocytes from Multiple Sclerosis Patients Edaravone Modulate Oxidative Stress in Multiple Sclerosis.Journal of central nervous system disease · 2022Article
- 4-Ethylguaiacol modulates neuroinflammation and Th1/Th17 differentiation to ameliorate disease severity in experimental autoimmune encephalomyelitis.Journal of neuroinflammation · 2021Article
- The Role of NADPH Oxidase in Neuronal Death and Neurogenesis after Acute Neurological Disorders.Antioxidants (Basel, Switzerland) · 2021Review
- White matter injury in infants with intraventricular haemorrhage: mechanisms and therapies.Nature reviews. Neurology · 2021Review
- Antigen presentation between T cells drives Th17 polarization under conditions of limiting antigen.Cell reports · 2021Article
- Neuregulin-1 beta 1 is implicated in pathogenesis of multiple sclerosis.Brain : a journal of neurology · 2021Article
Corrections and comments
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Authors and funding
12 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundTo evaluate the role of NADPH oxidase-mediated reactive oxygen species (ROS) production in multiple sclerosis pathogenesis, we examined the effects of apocynin, an NADPH oxidase assembly inhibitor, on experimental autoimmune encephalomyelitis (EAE).
methodsEAE was induced by immunization with myelin oligodendrocyte glycoprotein (MOG (35-55)) in C57BL/6 female mice. Three weeks after initial immunization, the mice were analyzed for demyelination, immune cell infiltration, and ROS production. Apocynin (30 mg/kg) was given orally once daily for the entire experimental course or after the typical onset of clinical symptom (15 days after first MOG injection).
resultsClinical signs of EAE first appeared on day 11 and reached a peak level on day 19 after the initial immunization. The daily clinical symptoms of EAE mice were profoundly reduced by apocynin. The apocynin-mediated inhibition of the clinical course of EAE was accompanied by suppression of demyelination, reduced infiltration by encephalitogenic immune cells including CD4, CD8, CD20, and F4/80-positive cells. Apocynin reduced MOG-induced pro-inflammatory cytokines in cultured microglia. Apocynin also remarkably inhibited EAE-associated ROS production and blood-brain barrier (BBB) disruption. Furthermore, the present study found that post-treatment with apocynin also reduced the clinical course of EAE and spinal cord demyelination.
conclusionsThese results demonstrate that apocynin inhibits the clinical features and neuropathological changes associated with EAE. Therefore, the present study suggests that inhibition of NADPH oxidase activation by apocynin may have a high therapeutic potential for treatment of multiple sclerosis pathogenesis.
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