Protective effect of ethyl vanillin against Aβ-induced neurotoxicity in PC12 cells via the reduction of oxidative stress and apoptosis

Increased aggregation of β-amyloid (Aβ) peptides induces oxidative stress, which is considered a major contributor in the development of Alzheimer's disease (AD). Prevention of Aβ-induced neurotoxicity is proposed as a possible modality for treatment of AD. The present study aimed to elucidate possible effects of ethyl vanillin (EVA), an analog of vanillin isolated from vanilla beans, on the Aβ(1-42)-induced oxidative injury in PC12 cells. EVA restrained the decrease in PC12 cell viability and apoptosis induction caused by treatment with Aβ(1-42). In addition, EVA markedly alleviated intracellular lipid peroxidation as demonstrated by malondialdehyde levels and reactive oxygen species production in Aβ(1-42)-treated PC12 cells. In addition, the reduction in the activity levels of the antioxidative enzymes superoxide dismutase, catalase and glutathione peroxidase was detected in Aβ(1-42)-treated PC12 cells. This effect was partially reversed by treatment with EVA. Furthermore, the results indicated that EVA attenuated Aβ(1-42)-induced caspase-3 activation and the increase noted in the apoptosis regulator Bcl-2/apoptosis regulator Bax ratio of PC12 cells. These results indicated that EVA could be used as an efficient and novel agent for the prevention of neurodegenerative diseases via inhibition of oxidative stress and cell apoptosis.