Coenzyme Q10 protects neural stem cells against hypoxia by enhancing survival signals

Brain Res. 2012 Oct 10;1478:64-73. doi: 10.1016/j.brainres.2012.08.025. Epub 2012 Aug 21.


Recanalization and secondary prevention are the main therapeutic strategies for acute ischemic stroke. Neuroprotective therapies have also been investigated despite unsuccessful clinical results. Coenzyme Q10 (CoQ10), which is an essential cofactor for electron transport in mitochondria, is known to have an antioxidant effect. We investigated the protective effects of CoQ10 against hypoxia in neural stem cells (NSCs). We measured cell viability and levels of intracellular signaling proteins after treatment with several concentrations of CoQ10 under hypoxia-reperfusion. CoQ10 protected NSCs against hypoxia-reperfusion in a concentration-dependent manner by reducing growth inhibition and inhibiting free radical formation. It increased the expression of a number of survival-related proteins such as phosphorylated Akt (pAkt), phosphorylated glycogen synthase kinase 3-β (pGSK3-β), and B-cell lymphoma 2 (Bcl-2) in NSCs injured by hypoxia-reperfusion and reduced the expression of death-related proteins such as cleaved caspase-3. We conclude that CoQ10 has effects against hypoxia-reperfusion induced damage to NSCs by enhancing survival signals and decreasing death signals.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Antioxidants / pharmacology*
  • Blotting, Western
  • Cell Hypoxia / drug effects
  • Cell Survival / drug effects
  • Cells, Cultured
  • Free Radicals / metabolism
  • In Situ Nick-End Labeling
  • Neural Stem Cells / cytology
  • Neural Stem Cells / drug effects*
  • Neural Stem Cells / metabolism*
  • Rats
  • Reperfusion Injury / metabolism
  • Signal Transduction / drug effects*
  • Ubiquinone / analogs & derivatives*
  • Ubiquinone / pharmacology


  • Antioxidants
  • Free Radicals
  • Ubiquinone
  • coenzyme Q10