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

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 A beta-induced rat model of AD, by studying A beta(1-40)-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 A beta(1-40)-induced increase of I-Ca can be inhibited by EDA in a dose-dependent manner. Treatment with EDA significantly improved A beta(1-40)-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 A beta(1-40) group. These results demonstrate that EDA can inhibit the neurotoxic effect of A beta toxicity. Collectively, these findings suggest that EDA may serve as a potential complemental treatment strategy for AD.