Amyloid-β-peptide (Aβ) deposition within the brains of Alzheimer’s disease (AD) patients results in the neurodegeneration. The peroxisome proliferator-activated receptor α (PPARα) is a lipid activated transcription factor, which controls the promoters of multiple genes encoding enzymes in the lipid metabolic pathways. Recent studies showed that the PPARαL162V polymorphism increased the risk of AD. In this study we determined the effect of activation of PPARα by Wy14643 on Aβ42-induced NT2N (NTera2 neurons) neurotoxicity. We found that the proportion of NT2N cells at Sub-G1 phase increased significantly in the Aβ42+Wy14643 group, compared to Aβ42 group after 24 hours of treatment. As to the extent of apoptosis, caspase 3 protein level, pGsk-3β/Gsk-3β ratio, and Bcl-2/Bax ratio were not significantly different between the Aβ42 group and the Aβ42+Wy14643 group. However, the addition of Wy14643 plus Aβ42 significantly increased the expression of endonuclease G (Endo G) protein, compared to the Aβ42 group. These results suggested that activation of PPARα did not influence the expression of caspase 3 protein, but significantly induced the expression of Endo G protein which accelerated the apoptosis of NT2N cells.
