Hypoxia Enhances β-Amyloid-Induced Apoptosis in Rat Cultured Hippocampal Neurons

Nobuaki Egashira; Katsunori Iwasaki; Motoki Ishibashi; Izzetin Hatip-Al-Khatib; Benjamin Wolozin; Kenichi Mishima; Keiichi Irie; Michihiro Fujiwara

doi:10.1254/jjp.90.321

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Hypoxia Enhances β-Amyloid-Induced Apoptosis in Rat Cultured Hippocampal Neurons

Nobuaki Egashira, Katsunori Iwasaki, Motoki Ishibashi, Izzetin Hatip-Al-Khatib, Benjamin Wolozin, Kenichi Mishima, Keiichi Irie, Michihiro Fujiwara

Author information

Nobuaki Egashira
Department of Neuropharmacology, Faculty of Pharmaceutical Sciences, Fukuoka University
Advanced Materials Institute, Fukuoka University
Katsunori Iwasaki
Department of Neuropharmacology, Faculty of Pharmaceutical Sciences, Fukuoka University
Advanced Materials Institute, Fukuoka University
Motoki Ishibashi
Department of Neuropharmacology, Faculty of Pharmaceutical Sciences, Fukuoka University
Izzetin Hatip-Al-Khatib
Department of Neuropharmacology, Faculty of Pharmaceutical Sciences, Fukuoka University
Advanced Materials Institute, Fukuoka University
Benjamin Wolozin
Advanced Materials Institute, Fukuoka University
Department of Pharmacology, Loyola University Medical Center
Kenichi Mishima
Department of Neuropharmacology, Faculty of Pharmaceutical Sciences, Fukuoka University
Keiichi Irie
Department of Neuropharmacology, Faculty of Pharmaceutical Sciences, Fukuoka University
Michihiro Fujiwara
Department of Neuropharmacology, Faculty of Pharmaceutical Sciences, Fukuoka University
Advanced Materials Institute, Fukuoka University

Keywords: β-Amyloid, Hypoxia, Apoptosis, MK-801, CNQX

JOURNAL FREE ACCESS

2002 Volume 90 Issue 4 Pages 321-327

DOI https://doi.org/10.1254/jjp.90.321

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Abstract

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.

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