Coenzyme Q10 attenuated beta-amyloid(25-35)-induced inflammatory responses in PC12 cells through regulation of the NF-kappa B signaling pathway

Abstract

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 A beta(25-35)-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 A beta(25-35)-injured PC12 cells. These inhibitions appeared to correlate with the suppression of NF-x3 activation by CoQ10, as pretreating PC12 cells with CoQ10 blocked the translocation of NF-icE. into the nuclear compartment and degradation of the inhibitory subunit MI Overall, these results implied that CoQ10 attenuated neuroinflammatory responses through the inactivation of NF-icIl dependent inflammatory pathways in 1025-35-induced PC12 cells. Therefore, CoQ10 may have therapeutic potential for neurodegenerative diseases by inhibiting pro-inflammatory mediators production.