Protective Effects of Coenzyme Q10 Against Hydrogen Peroxide-Induced Oxidative Stress in PC12 Cell: The Role of Nrf2 and Antioxidant Enzymes
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Oxidative stress is a major component of harmful cascades activated in neurodegenerative disorders. Coenzyme Q10 (CoQ10), an essential component in the mitochondrial respiratory chain, has recently gained attention for its potential role in the treatment of neurodegenerative disease. Here, we investigated the possible protective effects of CoQ10 on H2O2-induced neurotoxicity in PC12 cells and the underlying mechanism. CoQ10 showed high free radical-scavenging activity as measured by a DPPH and TEAC. Pre-treatment of cells with CoQ10 diminished intracellular generation of ROS in response to H2O2. H2O2 decreased viability of PC12 cells which was reversed by pretreatment with CoQ10 according to MTT assay. H2O2-induced lipid peroxidation was attenuated by CoQ10 as shown by inhibition of MDA formation. Furthermore, pre-incubation of the cells with CoQ10 also restored the activity of cellular antioxidant enzymes which had been altered by H2O2. Moreover, CoQ10 induced Nrf2 nuclear translocation, the upstream of antioxidant enzymes. These findings suggest CoQ10 augments cellular antioxidant defense capacity through both intrinsic free radical-scavenging activity and activation of Nrf2 and subsequently antioxidant enzymes induction, thereby protecting the PC12 cells from H2O2-induced oxidative cytotoxicity.
KeywordsCoenzyme Q10 Antioxidant enzyme Nrf2 Neurodegeneration
We gratefully acknowledge financial support of this work by Guangdong Medical College foundation (No. B2011011), Zhanjiang Science and Technology Planning Project (No. 2012C3104018), Shenzhen Science and Technology Planning Project (No. 201302173), Innovation Experiment Program for University Students of Guangdong Medical College (LZDM011).
Conflict of interest
The authors declare that they have no conflict of interest.
This article does not contain any studies with human participants or animals performed by any of the authors.
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