In multiple sclerosis during periods of remission a limited degree of myelin repair can be observed mediated by oligodendroglial precursor cells. Phosphodiesterase inhibitors act as anti-inflammatory agents and might hold promise for future multiple sclerosis treatment. Aims:
To investigate whether phosphodiesterase inhibitors could also influence myelin repair. Methods:
We stimulated primary oligodendroglial precursor cells with cilostazol, rolipram and vinpocetine and assessed their effects on repair related cellular processes. Results:
We found that vinpocetine exerted a strong negative effect on myelin expression while cilostazol and rolipram did not show such effects. In addition, vinpocetine decreased morphological complexities suggesting an overall negative impact on oligodendroglial cell maturation. We provide evidence that this is not mediated via a blockade of phosphodiesterase-1 but rather by inhibition of IĸB kinase. Conclusion:
These findings suggest that vinpocetine via IĸB inhibition exerts a strong negative impact on oligodendroglial cell maturation and may therefore provide the rationale to restrict its application during periods of remission in multiple sclerosis patients. This is of particular interest since vinpocetine is widely used as a health supplement thought to act as a cognitive and memory enhancer for healthy people and patients with neurological or muscle diseases.
Dr. Patrick Küry
Department of Neurology
Heinrich-Heine-University, Moorenstrasse 5, D-40225 Düsseldorf (Germany)
Tel. +49 211 811 78 22, Fax +49 211 811 84 69, E-Mail: firstname.lastname@example.org
Accepted: July 4, 2012
Published online: August 01, 2012
Number of Print Pages : 12
Cellular Physiology and Biochemistry (International Journal of Experimental Cellular Physiology, Biochemistry and Pharmacology)
Vol. 30, No. 3, Year 2012 (Cover Date: August 2012)
Journal Editor: Guggino W. (Baltimore, Md.), Lang F. (Tübingen)
ISSN: 1015-8987 (Print), eISSN: 1421-9778 (Online)
For additional information: http://www.karger.com/CPB
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