Inhibition of NADPH oxidase activation reduces EAE-induced white matter damage in mice

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dc.contributor.authorChoi, Bo Y
dc.contributor.authorKim, Jin H
dc.contributor.authorKho, A R
dc.contributor.authorKim, In Y
dc.contributor.authorLee, Song H
dc.contributor.authorLee, Bo E
dc.contributor.authorChoi, Eunhi
dc.contributor.authorSohn, Min
dc.contributor.authorStevenson, Mackenzie
dc.contributor.authorChung, Tae N
dc.contributor.authorKauppinen, Tiina M
dc.contributor.authorSuh, Sang W
dc.date.accessioned2015-10-08T17:47:34Z
dc.date.available2015-10-08T17:47:34Z
dc.date.issued2015-05-28
dc.date.updated2015-10-06T22:53:47Z
dc.description.abstractAbstract Background To 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). Methods EAE 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). Results Clinical 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. Conclusions These 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.
dc.identifier.citationJournal of Neuroinflammation. 2015 May 28;12(1):104
dc.identifier.urihttp://dx.doi.org/10.1186/s12974-015-0325-5
dc.identifier.urihttp://hdl.handle.net/1993/30890
dc.language.rfc3066en
dc.rightsopen accessen_US
dc.rights.holderChoi et al.; licensee BioMed Central.
dc.titleInhibition of NADPH oxidase activation reduces EAE-induced white matter damage in mice
dc.typeJournal Article
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