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JNK and p38 MAPK regulate oxidative stress and the inflammatory response in chlorpyrifos-induced apoptosis

Title
JNK and p38 MAPK regulate oxidative stress and the inflammatory response in chlorpyrifos-induced apoptosis
Author
신인철
Keywords
Chlorpyrifos; Reactive oxidative species; Apoptosis; Mitogen activated protein kinase; Cyclooxygenase-2
Issue Date
2013-04
Publisher
Elsevier Ireland LTD
Citation
Toxicology letters, 2013, 218(3), P.235-245
Abstract
To investigate mechanisms of neuronal cell death in response to chlorpyrifos (CPF), a pesticide, we evaluated the regulation of ROS and COX-2 in human neuroblastoma SH-SY5Y cells treated with CPF. CPF treatment produced cytotoxic effects that appeared to involve an increase in ROS. In addition, CPF treatment activated MAPK pathways including JNK, ERK1/2, and p38 MAPK, and MAPK inhibitors abolished the cytotoxicity and reduced ROS generation. Our data demonstrate that CPF induced apoptosis involving MAPK activation through ROS production. Furthermore, after the CPF treatment, COX-2 expression increased. Interestingly, JNK and p38 MAPK inhibitors attenuated the CPF-induced COX-2 expression while an ERK1/2 inhibitor did not. These findings suggest that pathways involving JNK and p38 MAPK, but not ERK1/2, mediated apoptosis and are involved in the inflammatory response. In conclusion, the JNK and p38 MAPK pathways might be critical mediators in CPF-induced neuronal apoptosis by both generating ROS and up-regulating COX-2. Crown Copyright (c) 2013 Published by Elsevier Ireland Ltd. All rights reserved.
URI
https://www.sciencedirect.com/science/article/pii/S037842741300060X?via%3Dihubhttp://hdl.handle.net/20.500.11754/52449
ISSN
0378-4274
DOI
10.1016/j.toxlet.2013.02.003
Appears in Collections:
COLLEGE OF MEDICINE[S](의과대학) > ETC
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