NDLI: Edaravone Protects HT22 Neurons from $H_{2}O_{2}$-induced Apoptosis by Inhibiting the MAPK Signaling Pathway

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Edaravone Protects HT22 Neurons from $H_{2}O_{2}$-induced Apoptosis by Inhibiting the MAPK Signaling Pathway

Content Provider	Scilit
Author	Zhao, Zhong-Yan Luan, Ping Huang, Shi-Xiong Xiao, Song-Hua Zhao, Jia Zhang, Bei Gu, Bei-Bei Pi, Rong-Biao Liu, Jun
Copyright Year	2012
Description	Journal: CNS neuroscience & therapeutics Aims Oxidative stress is frequently implicated in the pathology of neurodegenerative diseases. This study aimed to investigate the effects and their underlying mechanism(s) of edaravone upon hydrogen peroxide $(H_{2}O_{2}$)–induced oxidative stress and apoptosis in HT22 cells, a murine hippocampal neuronal model. Methods HT22 cells were treated with $H_{2}O_{2}$ in the presence of various concentrations of edaravone or in its absence. A CCK-8 assay, Hoechst 33342 staining, and flow cytometry were used to detect cytotoxicity and apoptosis. In addition, the levels of reactive oxygen species (ROS) and the expression of Bcl-2, Bax, p-ERK 1/2, p-JNK, and p-P38 proteins in HT22 cells were examined. Results Exogenous $H_{2}O_{2}$ decreased cell viability in a concentration-dependent manner and was associated with increased apoptosis and ROS production. Moreover, $H_{2}O_{2}$ significantly activated and upregulated the expression of p-ERK 1/2, p-JNK, and p-P38, while edaravon protected HT22 cells against $H_{2}O_{2}$-induced injury by inhibiting the production of ROS and activating the MAPK signaling pathway. Conclusions Our results provide the first evidence that edaravone can protect $H_{2}O_{2}$-induced cell injury in HT22 neurons via its antioxidant action. These findings suggest that edaravone may be useful in the treatment of neurodegenerative disorders in which oxidative stress has been principally implicated.
Related Links	https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6493402/pdf
Ending Page	169
Page Count	7
Starting Page	163
e-ISSN	17555949
DOI	10.1111/cns.12044
Journal	CNS neuroscience & therapeutics
Issue Number	3
Volume Number	19
Language	English
Publisher	Wiley-Blackwell
Publisher Date	2012-12-18
Access Restriction	Open
Subject Keyword	Journal: CNS neuroscience & therapeutics Cell Tissue Engineering Ht22 Cells Hydrogen Peroxide Neurodegenerative Diseases Neuroprotective Effect Oxidative Stress
Content Type	Text
Resource Type	Article

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