| Article ID | Journal | Published Year | Pages | File Type |
|---|---|---|---|---|
| 2589787 | NeuroToxicology | 2012 | 6 Pages |
Oxidative stress plays critical roles in the pathogenic mechanisms of several neurodegenerative disorders including Alzheimer's disease (AD), thus much research effort has focused on antioxidants as potential treatment agents for AD. Coenzyme Q10 (CoQ10) is known to have powerful antioxidant effects. We investigated the neuroprotective effects of CoQ10 against Amyloid beta25–35 (Aβ25–35)-induced neurotoxicity in rat cortical neurons. To evaluate the neuroprotective effects of CoQ10 on Aβ25–35-injured neurons, primary cultured cortical neurons were treated with several concentrations of CoQ10 and/or Aβ25–35 for 48 h. CoQ10 protected neuronal cells against Aβ25–35-induced neurotoxicity in a concentration-dependent manner. These neuroprotective effects of CoQ10 were blocked by LY294002 (10 μM), a phosphatidylinositol 3-kinase (PI3K) inhibitor. Aβ25–35 concentration-dependent increased free radical levels in rat cortical neurons, while combined treatment with CoQ10 reduced these free radical levels in a dose-dependent manner. Meanwhile, CoQ10 treatment of Aβ25–35-injured primary cultured cortical neurons increased the expression levels of p85aPI3K, phosphorylated Akt, phosphorylated glycogen synthase kinase-3β, and heat shock transcription factor, which are proteins related to neuronal cell survival, and decreased the levels of cytosolic cytochrome c and cleaved caspase-3, which are associated with neuronal cell death. Together, these results suggest that the neuroprotective effects of CoQ10 on Aβ25–35 neurotoxicity are mediated by inhibition of oxidative stress together with activation of the PI3-K/Akt pathway.
► CoQ10 protected neuronal cells against Aβ25–35 and these effects were blocked by PI3K inhibitor. ► Aβ25–35 increased free radical levels in neuronal cells, while CoQ10 reduced these levels. ► Neuroprotective effects of CoQ10 are mediated by activation of the PI3K signaling pathway.
