Decursinol protects PC12 cells from β‐amyloid25‐35‐induced neurotoxicity via the activation of NF‐E2 related factor 2

Abstract

One of the pathological hallmarks of Alzheimer's disease is the progressive accumulation of beta‐amyloid(Aβ) and Aβ insult to neuronal cells has been identified as one of the major causes of the disease. Decursinol, found in the roots of Angelica gigas Nakai, has been traditionally used to treat anemia and other various diseases. In this study, we investigated protective effects of decursinol on beta‐amyloid25–35(Aβ25–35)‐induced cell death in PC12 cells. Following exposure PC12 cells to 25μM Aβ25–35 for 24 hrs significant increased the lipid peroxidation(MDA), decreased the activities of antioxidant enzymes(superoxide dismutase, glutathione peroxidase, catalase) and the level of glutathione(GST) content which were accompanied by decreased cell viability, activity of GST and transactivation of activator NF‐E2‐related factor‐2(Nrf2) which mediates GST gene transcription. Besides, pretreatment of PC12 cells with decursinol for 3 hrs significantly reversed the effect of Aβ by decreasing the oxidative stress and increasing the activation of Nrf2 and GST activity level. These data indicate decursinol protected PC12 cells against Aβ‐induced neurotoxicity through the inhibition of oxidative damage through activation of Nrf2.This research is supported by Biohealth Products Research Center(BPRC) of Inje University.