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Brain Res Bull. 2017 May;131:192-198. doi: 10.1016/j.brainresbull.2017.04.014. Epub 2017 Apr 27.

Coenzyme Q10 attenuated β-amyloid25-35-induced inflammatory responses in PC12 cells through regulation of the NF-κB signaling pathway.

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Dongguan Scientific Research Center, Guangdong Medical University, Dongguan 523-808, PR China.
The Second Affiliated Hospital of Liaoning University of Traditional Chinese Medicine Clinical Laboratory, 110-033, PR China.
Guangdong Runhe Co. Ltd., Guangzhou, 510-800, PR China.
Department of Chemical and Biomolecular Engineering, Korea Advanced Institute of Science and Technology, Republic of Korea. Electronic address:


Inflammation plays critical roles in the pathogenic mechanisms of several neurodegenerative disorders including Alzheimer's disease (AD). Previous study revealed that CoQ10 augmented cellular antioxidant defense capacity, thereby protecting PC12 cells from oxidative neurotoxicity. However, the mechanism by which CoQ10 inhibits inflammation remains unknown. In this study, we aim to examine the effects of CoQ10 on Aβ25-35-induced inflammatory in PC12 cells and the underlying molecular mechanism of its neuroprotective action. CoQ10 suppressed the protein expression of COX-2 and the level of PGE2 in Aβ25-35-injured PC12 cells. These inhibitions appeared to correlate with the suppression of NF-κB activation by CoQ10, as pretreating PC12 cells with CoQ10 blocked the translocation of NF-κB into the nuclear compartment and degradation of the inhibitory subunit IκB. Overall, these results implied that CoQ10 attenuated neuroinflammatory responses through the inactivation of NF-κB dependent inflammatory pathways in Aβ25-35-induced PC12 cells. Therefore, CoQ10 may have therapeutic potential for neurodegenerative diseases by inhibiting pro-inflammatory mediators production.


Coenzyme Q10; Inflammatory; NF–κB; β–amyloid(25–35)

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