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BioMed Research International
Volume 2014 (2014), Article ID 370368, 7 pages
Research Article

Inhibitory Effects of Edaravone in β-Amyloid-Induced Neurotoxicity in Rats

1Department of Neurology, Linyi People’s Hospital, Linyi City, Shandong 276000, China
2Department of Out-Patient, Yulin Teacher’s College Hospital, Yulin, Guangxi 537000, China
3Department of Neurology, Sun Yat-Sen Memorial Hospital, Sun Yat-Sen University, Guangdong 510120, China

Received 16 January 2014; Accepted 24 February 2014; Published 2 April 2014

Academic Editor: Jin-Tai Yu

Copyright © 2014 Feng He et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


Amyloid protein can damage nerve cells through a variety of biological mechanisms including oxidative stress, alterations in calcium homeostasis, and proapoptosis. Edaravone, a potent free radical scavenger possessing antioxidant effects, has been proved neuroprotective effect in stroke patients. The current study aimed to investigate the effects of EDA in an Aβ-induced rat model of AD, by studying Aβ1–40-induced voltage-gated calcium channel currents in hippocampal CA1 pyramidal neurons, learning and memory behavioral tests, the number of surviving cholinergic neurons in the basal forebrain, and the acetylcholine level in the hippocampus in this rat model of AD. The results showed that the Aβ1–40-induced increase of can be inhibited by EDA in a dose-dependent manner. Treatment with EDA significantly improved Aβ1–40-induced learning and memory performance. Choline acetyltransferase positive cells in basal forebrain and acetylcholine content in the hippocampus were increased by the administration of EDA as compared with the non-EDA treated Aβ1–40 group. These results demonstrate that EDA can inhibit the neurotoxic effect of Aβ toxicity. Collectively, these findings suggest that EDA may serve as a potential complemental treatment strategy for AD.