Analysis of gene expression in MOG-induced experimental autoimmune encephalomyelitis after treatment with a novel brain-penetrating antioxidant

Yossi Gilgun-Sherki, Yael Barhum, Daphne Atlas, Eldad Melamed, Daniel Offen*

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

Abstract

Accumulating data from experimental studies indicate that oxidative stress has a major role in the pathogenesis of multiple sclerosis (MS). It has been suggested that local production of reactive oxygen species, probably by macrophages, mediates axonal damage in both MS patients and the mouse model experimental autoimmune encephalomyelitis (EAE). We have shown previously that our novel brain-penetrating antioxidant, N-acetylcysteine amide (AD4), reduces the clinical and pathological symptoms, including inflammation and axonal damage in myelin oligodendrocyte glycoprotein (MOG)-induced chronic EAE in mice. The aim of this study was to examine the molecular mechanism by which AD4 exerts protection in MOG-induced EAE mice. Therefore, we analyzed gene-expression profile in the spinal cords of MOG-induced chronic EAE mice and compared them with MOG-induced mice treated with AD4, using a cDNA microarray. We found that MOG treatment up-regulated genes encoding growth factors, cytokines, death receptors, proteases, and myelin structure proteins, whereas MOG- and AD4-treated mice demonstrated gene expression profiles similar to that seen in naïve healthy mice. In conclusion, our study shows that chronic AD4 administration suppresses the induction of various pathological pathways that play a role in EAE and probably in MS.

Original languageEnglish
Pages (from-to)125-135
Number of pages11
JournalJournal of Molecular Neuroscience
Volume27
Issue number1
DOIs
StatePublished - Sep 2005

Keywords

  • AD4
  • Antioxidants
  • Experimental autoimmune encephalomyelitis (EAE)
  • Gene expression
  • Multiple sclerosis (MS)
  • Myelin oligodendrocyte glycoprotein (MOG)

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