The Japanese Journal of Pharmacology
Online ISSN : 1347-3506
Print ISSN : 0021-5198
ISSN-L : 0021-5198
Full Papers
Hypoxia Enhances β-Amyloid-Induced Apoptosis in Rat Cultured Hippocampal Neurons
Nobuaki EgashiraKatsunori IwasakiMotoki IshibashiIzzetin Hatip-Al-KhatibBenjamin WolozinKenichi MishimaKeiichi IrieMichihiro Fujiwara
キーワード: β-Amyloid, Hypoxia, Apoptosis, MK-801, CNQX
ジャーナル フリー

2002 年 90 巻 4 号 p. 321-327


We investigated the effect of hypoxia on β-amyloid (Aβ)-induced apoptosis in rat cultured hippocampal neurons. Aβ (25 μM for 48 h) decreased the number of neuronal cells and increased the number of TUNEL-positive cells. Hypoxia (6 h) also decreased the number of neuronal cells, but did not increase the number of TUNEL-positive cells. Moreover, combined treatment with both Aβ and hypoxia (Aβ/hypoxia) significantly enhanced the decrease in the number of neuronal cells and the increase in the number of TUNEL-positive cells. Z-Asp-CH2-DCB, an inhibitor of interleukin-1β-converting enzyme (ICE), or 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX), a non-N-methyl-D-aspartate (non-NMDA) receptor antagonist, decreased the number of TUNEL-positive cells with Aβ/hypoxia. These findings suggest that ischemia or hypoxia is an important factor that facilitates the symptoms of Alzheimer’s disease and that non-NMDA receptors are involved in the induction of apoptosis in patients suffering from both cerebrovascular disease and Alzheimer’s disease.

© The Japanese Pharmacological Society 2002
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