COX 2 for MS

A board to discuss future MS therapies in early stage (Phase I or II) trials.

COX 2 for MS

Postby bromley » Tue Aug 01, 2006 7:45 am

Another cure for those pesky mice with MS. Next time you visit your neuro ask if MD stands for Mouse Doctor. How do they get mice to stay still in the MRI tunnel?
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Postby carolew » Tue Aug 01, 2006 1:40 pm

Not long ago, I asked why they didn't give us anti-inflammatories, I guess someone else asked himself the same question.... Carole :?
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Re: COX 2 for MS

Postby NHE » Sat Aug 05, 2006 2:37 am

Thanks Bromley. This article appears to provide more justification for limiting dietary saturated fatty acids. In effect, reducing the activity of the arachadonic acid pathway while increasing the omega-3 pathway via docosahexaenoic acid. In addition, it also provides positive rationale for supplements such as green tea and curcumin both of which have been widely reported to have anti-inflammatory activity.

Here's the full citation...
    Selective COX-2 inhibitor celecoxib prevents experimental autoimmune encephalomyelitis through COX-2-independent pathway. Brain. 2006, 129(Pt 8):1984-92.

    Cyclooxygenase (COX) is a key enzyme of arachidonic acid metabolism and exists as two distinct isoforms. COX-1 is constitutively expressed in most tissues, whereas COX-2 is inducibly expressed at the site of inflammation. Selective inhibitors of COX-2 have been developed and have been used as anti-inflammatory agents. Here, we show that a new-generation COX-2 inhibitor, celecoxib, inhibited experimental autoimmune encephalomyelitis (EAE). Celecoxib, but not other COX-2 inhibitors such as nimesulid, prevented myelin oligodendrocyte glycoprotein (MOG) induced EAE when administrated orally on the day of disease induction. Moreover, celecoxib inhibited EAE in COX-2-deficient mice, indicating that celecoxib inhibited EAE in a COX-2-independent manner. In celecoxib-treated mice, interferon-gamma (IFN-gamma) production from MOG-specific T cells was reduced and MOG-specific IgG1 was elevated compared with vehicle-treated mice. Infiltration of inflammatory cells into the central nervous system and the expression of adhesion molecules, P-selectin and intercellular adhesion molecule-1 (ICAM-1), and a chemokine, monocyte chemoattractant peptide-1 (MCP-1), were inhibited when mice were treated with celecoxib. These results suggest that celecoxib may be useful as a new additional therapeutic agent for multiple sclerosis.

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