Effect of Antioxidant Flavanone, Naringenin, fromCitrus junoson Neuroprotection

Abstract

Amyloid β protein (Aβ)-induced free radical-mediated neurotoxicity is known as a leading hypothesis for a cause of Alzheimer's disease. Aβ increased free radical production and lipid peroxidation in PC12 nerve cells, resulting in apoptosis and cell death. The protective effect of naringenin, a major flavanone constituent isolated from Citrus junos, against Aβ-induced neurotoxicity was investigated using PC12 cells. Pretreatment with isolated naringenin and vitamin C prevented the generation of the Aβ-induced reactive oxygen species. Naringenin resulted in the decrease of Aβ toxicity in a manner of concentration dependence, which was assessed by the 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay. However, treatment with these antioxidants inhibited the Aβ-induced neurotoxic effect. The antiamnestic activity of naringenin in vivo was also evaluated using ICR mice with amnesia induced by scopolamine (1 mg/kg body weight). Naringenin, when administered to ICR mice at 4.5 mg/kg body weight, significantly ameliorated scopolamine-induced amnesia as measured in the passive avoidance test. Therefore, these results indicate that micromolecular Aβ-induced in vitro oxidative cell stress is reduced by naringenin and naringenin may be a useful chemopreventive agent against a neurodegenerative disease such as Alzheimer's disease. Keywords: Naringenin; oxidative stress; Alzheimer's disease; antiamnestic agent