title: Vinpocetine inhibits oligodendroglial precursor cell differentiation.
abstract: BACKGROUND
  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.
  
  
  OBJECTIVE
  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.
  
  
  CONCLUSIONS
  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.
authors.affiliation: Heinrich-Heine-University, Medical Faculty, Department of Neurology, Düsseldorf, Germany.
authors.forename: Klintsy Julieta
authors.initials: KJ
authors.lastname: Torres
authors.forename: Peter
authors.initials: P
authors.lastname: Göttle
authors.forename: David
authors.initials: D
authors.lastname: Kremer
authors.forename: Jose Flores
authors.initials: JF
authors.lastname: Rivera
authors.forename: Lucinda
authors.initials: L
authors.lastname: Aguirre-Cruz
authors.forename: Teresa
authors.initials: T
authors.lastname: Corona
authors.forename: Hans-Peter
authors.initials: HP
authors.lastname: Hartung
authors.forename: Patrick
authors.initials: P
authors.lastname: Küry
mesh_terms: D000818:Animals; D002454:Cell Differentiation / Q000187:drug effects*; D002478:Cells, Cultured; D054377:Chemokine CXCL12 / Q000378:metabolism; D000077407:Cilostazol; D005786:Gene Expression Regulation / Q000187:drug effects; D051550:I-kappa B Kinase / Q000378:metabolism; D009186:Myelin Sheath / Q000235:genetics / Q000378:metabolism; D009836:Oligodendroglia / Q000166:cytology / Q000378:metabolism*; D010726:Phosphodiesterase Inhibitors / Q000494:pharmacology*; D051381:Rats; D020889:Rolipram / Q000494:pharmacology; D013777:Tetrazoles / Q000494:pharmacology; D014748:Vinca Alkaloids / Q000494:pharmacology*
chemical_list: D054377:Chemokine CXCL12; D010726:Phosphodiesterase Inhibitors; D013777:Tetrazoles; D014748:Vinca Alkaloids; C013983:vinpocetine; D051550:I-kappa B Kinase; D020889:Rolipram; D000077407:Cilostazol