Protective Effect of Edaravone in Primary Cerebellar Granule Neurons against Iodoacetic Acid-Induced Cell Injury

Edaravone (EDA) is clinically used for treatment of acute ischemic stroke in Japan and China due to its potent free radical-scavenging effect. However, it has yet to be determined whether EDA can attenuate iodoacetic acid- (IAA-) induced neuronal death in vitro. In the present study, we investigated...

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Bibliographic Details
Published in:Oxidative medicine and cellular longevity 2015-01, Vol.2015 (2015), p.1-8
Main Authors: Wang, Yuqiang, Yu, Pei, Zhang, Zai Jun, Sun, Yewei, Zhang, Gaoxiao, Guo, Baojian, Wang, Liang, Zhu, Longjun, Zhou, Xinhua, Lee, Simon Ming-Yuen
Format: Article
Language:English
Subjects:
Animals
Antipyrine - analogs & derivatives
Antipyrine - pharmacology
Apoptosis
Apoptosis - drug effects
Brain research
Caspase 3 - metabolism
Cell Survival - drug effects
Cells, Cultured
Chinese medicine
Dehydrogenases
Electronic design automation
Enzymes
Free radicals
Glucose
Hypoxia
Iodoacetic Acid - toxicity
Ischemia
Laboratories
Medical research
Membrane Potential, Mitochondrial - drug effects
Microscopy, Fluorescence
Neurons
Neurons - cytology
Neurons - drug effects
Neurons - metabolism
Neuroprotective Agents - pharmacology
Oxidative stress
Rats
Rats, Sprague-Dawley
Rodents
Science
Stroke (Disease)
Studies
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Summary:Edaravone (EDA) is clinically used for treatment of acute ischemic stroke in Japan and China due to its potent free radical-scavenging effect. However, it has yet to be determined whether EDA can attenuate iodoacetic acid- (IAA-) induced neuronal death in vitro. In the present study, we investigated the effect of EDA on damage of IAA-induced primary cerebellar granule neurons (CGNs) and its possible underlying mechanisms. We found that EDA attenuated IAA-induced cell injury in CGNs. Moreover, EDA significantly reduced intracellular reactive oxidative stress production, loss of mitochondrial membrane potential, and caspase 3 activity induced by IAA. Taken together, EDA protected CGNs against IAA-induced neuronal damage, which may be attributed to its antiapoptotic and antioxidative activities.
ISSN:1942-0900
1942-0994
DOI:10.1155/2015/606981