Idebenone protects
hippocampal neurons against amyloid beta-peptide-induced neurotoxicity in rat
primary cultures.
Hirai K, Hayako H, Kato K, Miyamoto M.
Pharmaceutical Research Division,
Takeda Chemical Industries Ltd., Osaka,
Japan
Naunyn Schmiedebergs Arch Pharmacol 1998 Nov;358(5):582-5
ABSTRACT
The application of amyloid
beta-peptide (Abeta) 1-40 (10 microM) 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
Abeta1-40(10 microM)-induced neurotoxicity. To determine the morphological
change in neurons during the Abeta1-40-induced cytotoxicity, the cells were
immunostained with anti-MAP2 antibodies. After 4-day exposure to 10 microM
Abeta1-40, 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 Abeta1-40, 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 Abeta1-40, and idebenone protects
neurons against the Abeta1-40-induced neurotoxicity.
