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Estrogen blocks neurotoxic effects of beta-amyloid (1-42) and induces neurite extension on B103 cells.

Mook-Jung, I; Joo, I; Sohn, S; Kwon, HJ; Huh, K; Jung, MW
Neuroscience letters, 235(3):101-104, 1997
Journal Title
Neuroscience letters
Clinical studies have shown that estrogen replacement therapy is associated with reduced risk of Alzheimer's disease (AD). We tested whether or not estrogen blocks neurotoxic effects of beta-amyloid (1-42) (A beta1-42) on cultured B103 cells. A beta1-42 (1 microM) induced typical necrotic cell death, as revealed by light and electron microscopic examinations. Co-administration of estrogen not only blocked A beta1-42 toxicity to a large degree, but also enhanced neurite extension. Pretreatment with estrogen was even more effective in blocking A beta1-42 toxicity. When added 18 h after the beginning of A beta1-42 treatment, estrogen was still effective in halting the progress of cell death and enhancing neurite extension. The protection against A beta1-42-induced neuronal death by estrogen was unlikely due to a blockade of lipid peroxidation injury, since estrogen completely failed to attenuate ferrous chloride-induced cell death. These results demonstrate that estrogen blocks A beta1-42-induced neurotoxicity and enhances neurite extension on B103 cells, both of which may well be underlying mechanisms of beneficial effects of estrogen in AD.
MeSH terms
Amyloid beta-Peptides/antagonists & inhibitors/*toxicityAnimalsBrain/cytology/*drug effectsCell LineEstrogens/*pharmacologyNeurites/*drug effectsNeurons/*drug effects/ultrastructureNeurotoxins/*toxicityPeptide Fragments/antagonists & inhibitors/*toxicityRats
Appears in Collections:
Journal Papers > School of Medicine / Graduate School of Medicine > Microbiology
Journal Papers > Research Organization > Institute for Medical Sciences
Journal Papers > School of Medicine / Graduate School of Medicine > Neurology
AJOU Authors
주, 인수손, 성향허, 균정, 민환
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