2-BFI ameliorates EAE-induced mouse spinal cord damage: effective therapeutic time window and possible mechanisms

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DOIResolve DOI: http://doi.org/10.1016/j.brainres.2012.09.016
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TypeArticle
Journal titleBrain Research
ISSN0006-8993
Volume1483
Pages1319; # of pages: 7
SubjectEAE; 2-BFI; Inflammatory cytokines; IL-17; IFN-γ; IL-10; Multiple sclerosis; Therapeutic time window
AbstractOur previous studies showed that ligands to type 2 imidazoline receptors (I2R), including 2-(2-Benzofuranyl)-2-imidazoline (2-BFI) and Idazoxan, were effective in reducing spinal cord inflammation caused by experimental autoimmune encephalomyelitis (EAE). In the present study, we determined the effective therapeutic time window of 2-BFI and found that administration of 2-BFI in mice before the appearance of ascending flaccid paralysis (1–10 days post immunization), but not during the period when neurological deficits occurred (11–20 days post immunization), significantly ameliorated EAE-induced neurobehavioral deficits, reduced the infiltration of inflammatory cells into the spinal cord, and reduced the level of demyelination. More interestingly, giving 2-BFI during 1–10 days post immunization selectively suppressed IL-17 levels in the peripheral blood, which strongly suggests that IL-17 may be a good early marker to indicate EAE progression and that 2-BFI may target CD4+ T lymphocytes, especially Th17 cells to reduce IL-17 expression. Collectively, these studies led us to envisage that 2-BFI can be a useful drug to treat multiple sclerosis (MS) when used in combination with an early indicator of MS progression, such as IL-17.
Publication date
PublisherElsevier
LanguageEnglish
AffiliationHuman Health Therapeutics; National Research Council Canada
Peer reviewedYes
IdentifierS0006899312014795
NPARC number21268678
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Record identifier4da8f65d-4e7a-4735-8a5c-6c230af0fdff
Record created2013-11-07
Record modified2016-05-09
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