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Eckol protects V79-4 lung fibroblast cells against gamma-ray radiation-induced apoptosis via the scavenging of reactive oxygen species and inhibiting of the c-Jun NH(2)-terminal kinase pathway

Cited 47 time in Web of Science Cited 48 time in Scopus
Authors
Zhang, Rui; Kang, Kyoung Ah; Piao, Mei Jing; Ko, Dong Ok; Wang, Zhi Hong; Lee, In Kyung; Kim, Bum Joon; Jeong, Il Yun; Shin, Taekyun; Park, Jae Woo; Lee, Nam Ho; Hyun, Jin Won
Issue Date
2008-07-16
Publisher
Elsevier
Citation
Eur J Pharmacol. 2008 Sep 4;591(1-3):114-23. Epub 2008 Jun 28.
Keywords
AnimalsApoptosis/drug effects/radiation effectsCell LineCell Survival/drug effects/radiation effectsCricetinaeCricetulusDNA Damage/drug effects/radiation effectsDioxins/*pharmacologyFibroblasts/drug effects/radiation effectsFree Radical Scavengers/pharmacologyGamma Rays/*adverse effectsJNK Mitogen-Activated Protein Kinases/metabolismLung/cytology/drug effects/radiation effectsMAP Kinase Kinase 4/drug effects/radiation effectsOxidative Stress/*drug effects/radiation effectsReactive Oxygen Species/*metabolismTranscription Factor AP-1/drug effects/radiation effects
Abstract
The radioprotective effect of eckol against gamma-ray radiation-induced oxidative stress and its possible protective mechanisms were investigated. Eckol was found to reduce the intracellular reactive oxygen species generated by gamma-ray radiation. Moreover, eckol also protected against radiation-induced cellular DNA damage and membrane lipid peroxidation, which are the main targets of radiation-induced damage. In addition, eckol recovered the cell viability damaged by radiation via the inhibition of apoptosis. Irradiated cells with eckol treatment reduced the expression of bax, the activation of caspase 9 and caspase 3, which were induced by radiation. However, irradiated cells with eckol recovered the expression of bcl-2 and mitochondrial cytochrome c which were decreased by radiation. The anti-apoptotic effect of eckol exerted via the inhibition of mitogen-activated protein kinase kinase-4 (MKK4/SEK1)-c-Jun NH(2)-terminal kinase (JNK)-activator protein 1 (AP-1) cascades induced by radiation. In summary, the results suggest that eckol protects cells against the oxidative stress induced by radiation via the reduction of reactive oxygen species and the attenuation of activation in SEK1-JNK-AP-1 pathway.
ISSN
0014-2999 (Print)
Language
English
URI
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=18625217

http://www.sciencedirect.com/science?_ob=MImg&_imagekey=B6T1J-4SVV8MD-1-W&_cdi=4892&_user=168665&_orig=search&_coverDate=09%2F04%2F2008&_sk=994089998&view=c&wchp=dGLbVlz-zSkWA&md5=90ebbbdeed08eeff28be7f7237fe6d95&ie=/sdarticle.pdf

https://hdl.handle.net/10371/46294
DOI
https://doi.org/10.1016/j.ejphar.2008.06.086
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College of Medicine/School of Medicine (의과대학/대학원)Microbiology (미생물학전공)Journal Papers (저널논문_미생물학전공)
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