Idebenone protects hippocampal neurons against amyloid β-peptide-induced neurotoxicity in rat primary cultures

Abstract

The application of amyloid β-peptide (Aβ) 1–40 (10 µM) caused neurodegeneration of hippocampal neuronal cells, as indicated by the release of lactate dehydrogenase (LDH) into the culture medium. Treatment with idebenone (10–1000 nM), a potent antioxidant in mitochondria, protected the hippocampal neurons against the Aβ1–40 (10 µM)-induced neurotoxicity. To determine the morphological change in neurons during the Aβ1–40-induced cytotoxicity, the cells were immunostained with anti-MAP2 antibodies. After 4-day exposure to 10 µM Aβ1–40, the number of neurons was reduced, and the surviving neurons had an apparently reduced number of neurites which were shorter than those of control neurons. When idebenone was added to the culture medium with Aβ1–40, the number of surviving neurons was significantly increased, and their neurites were as long as seen in control culture. These results suggest that reactive oxygen species mediate neurotoxicity of Aβ1–40, and idebenone protects neurons against the Aβ1–40-induced neurotoxicity.