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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Main Authors: Xinhua Zhou, Longjun Zhu, Liang Wang, Baojian Guo, Gaoxiao Zhang, Yewei Sun, Zaijun Zhang, Simon Ming-Yuen Lee, Pei Yu, Yuqiang Wang
Format: Article
Language:English
Published: Hindawi Limited 2015-01-01
Series:Oxidative Medicine and Cellular Longevity
Online Access:http://dx.doi.org/10.1155/2015/606981
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spelling doaj-5071c9e98ab04f7e8bf365525a31d4af2020-11-25T00:36:00ZengHindawi LimitedOxidative Medicine and Cellular Longevity1942-09001942-09942015-01-01201510.1155/2015/606981606981Protective Effect of Edaravone in Primary Cerebellar Granule Neurons against Iodoacetic Acid-Induced Cell InjuryXinhua Zhou0Longjun Zhu1Liang Wang2Baojian Guo3Gaoxiao Zhang4Yewei Sun5Zaijun Zhang6Simon Ming-Yuen Lee7Pei Yu8Yuqiang Wang9Institute of New Drug Research and Guangdong Province Key Laboratory of Pharmacodynamic Constituents of Traditional Chinese Medicine, Jinan University College of Pharmacy, Guangzhou 510632, ChinaInstitute of New Drug Research and Guangdong Province Key Laboratory of Pharmacodynamic Constituents of Traditional Chinese Medicine, Jinan University College of Pharmacy, Guangzhou 510632, ChinaInstitute of New Drug Research and Guangdong Province Key Laboratory of Pharmacodynamic Constituents of Traditional Chinese Medicine, Jinan University College of Pharmacy, Guangzhou 510632, ChinaInstitute of New Drug Research and Guangdong Province Key Laboratory of Pharmacodynamic Constituents of Traditional Chinese Medicine, Jinan University College of Pharmacy, Guangzhou 510632, ChinaInstitute of New Drug Research and Guangdong Province Key Laboratory of Pharmacodynamic Constituents of Traditional Chinese Medicine, Jinan University College of Pharmacy, Guangzhou 510632, ChinaInstitute of New Drug Research and Guangdong Province Key Laboratory of Pharmacodynamic Constituents of Traditional Chinese Medicine, Jinan University College of Pharmacy, Guangzhou 510632, ChinaInstitute of New Drug Research and Guangdong Province Key Laboratory of Pharmacodynamic Constituents of Traditional Chinese Medicine, Jinan University College of Pharmacy, Guangzhou 510632, ChinaState Key Laboratory of Quality Research in Chinese Medicine and Institute of Chinese Medical Sciences, University of Macau, Avenue Padre Tomás Pereira S.J., MacauInstitute of New Drug Research and Guangdong Province Key Laboratory of Pharmacodynamic Constituents of Traditional Chinese Medicine, Jinan University College of Pharmacy, Guangzhou 510632, ChinaInstitute of New Drug Research and Guangdong Province Key Laboratory of Pharmacodynamic Constituents of Traditional Chinese Medicine, Jinan University College of Pharmacy, Guangzhou 510632, ChinaEdaravone (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.http://dx.doi.org/10.1155/2015/606981
collection DOAJ
language English
format Article
sources DOAJ
author Xinhua Zhou
Longjun Zhu
Liang Wang
Baojian Guo
Gaoxiao Zhang
Yewei Sun
Zaijun Zhang
Simon Ming-Yuen Lee
Pei Yu
Yuqiang Wang
spellingShingle Xinhua Zhou
Longjun Zhu
Liang Wang
Baojian Guo
Gaoxiao Zhang
Yewei Sun
Zaijun Zhang
Simon Ming-Yuen Lee
Pei Yu
Yuqiang Wang
Protective Effect of Edaravone in Primary Cerebellar Granule Neurons against Iodoacetic Acid-Induced Cell Injury
Oxidative Medicine and Cellular Longevity
author_facet Xinhua Zhou
Longjun Zhu
Liang Wang
Baojian Guo
Gaoxiao Zhang
Yewei Sun
Zaijun Zhang
Simon Ming-Yuen Lee
Pei Yu
Yuqiang Wang
author_sort Xinhua Zhou
title Protective Effect of Edaravone in Primary Cerebellar Granule Neurons against Iodoacetic Acid-Induced Cell Injury
title_short Protective Effect of Edaravone in Primary Cerebellar Granule Neurons against Iodoacetic Acid-Induced Cell Injury
title_full Protective Effect of Edaravone in Primary Cerebellar Granule Neurons against Iodoacetic Acid-Induced Cell Injury
title_fullStr Protective Effect of Edaravone in Primary Cerebellar Granule Neurons against Iodoacetic Acid-Induced Cell Injury
title_full_unstemmed Protective Effect of Edaravone in Primary Cerebellar Granule Neurons against Iodoacetic Acid-Induced Cell Injury
title_sort protective effect of edaravone in primary cerebellar granule neurons against iodoacetic acid-induced cell injury
publisher Hindawi Limited
series Oxidative Medicine and Cellular Longevity
issn 1942-0900
1942-0994
publishDate 2015-01-01
description 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.
url http://dx.doi.org/10.1155/2015/606981
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