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

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. PMID: 28458038 [PubMed - as supplied by publisher]
Source: Brain Research Bulletin - Category: Neurology Authors: Tags: Brain Res Bull Source Type: research