JNK and p38 MAPK regulate oxidative stress and the inflammatory response in chlorpyrifos-induced apoptosis
- Authors
- Ki, Yeo-Woon; Park, Jae Hyeon; Lee, Jeong Eun; Shin, In Chul; Koh, Hyun Chul
- Issue Date
- Apr-2013
- Publisher
- ELSEVIER IRELAND LTD
- Keywords
- Chlorpyrifos; Reactive oxidative species; Apoptosis; Mitogen activated protein kinase; Cyclooxygenase-2
- Citation
- TOXICOLOGY LETTERS, v.218, no.3, pp.235 - 245
- Indexed
- SCIE
SCOPUS
- Journal Title
- TOXICOLOGY LETTERS
- Volume
- 218
- Number
- 3
- Start Page
- 235
- End Page
- 245
- URI
- https://scholarworks.bwise.kr/hanyang/handle/2021.sw.hanyang/163127
- DOI
- 10.1016/j.toxlet.2013.02.003
- ISSN
- 0378-4274
- 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.
- Files in This Item
-
Go to Link
- Appears in
Collections - 서울 의과대학 > 서울 약리학교실 > 1. Journal Articles
![qrcode](https://api.qrserver.com/v1/create-qr-code/?size=55x55&data=https://scholarworks.bwise.kr/hanyang/handle/2021.sw.hanyang/163127)
Items in ScholarWorks are protected by copyright, with all rights reserved, unless otherwise indicated.