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.
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.
Zhang
Rui
R
Department of Biochemistry, College of Medicine and Applied Radiological Science Research Institute, Cheju National University, Jeju-si 690-756, Republic of Korea.
Kang
Kyoung Ah
KA
Piao
Mei Jing
MJ
Ko
Dong Ok
DO
Wang
Zhi Hong
ZH
Lee
In Kyung
IK
Kim
Bum Joon
BJ
Jeong
Il Yun
IY
Shin
Taekyun
T
Park
Jae Woo
JW
Lee
Nam Ho
NH
Hyun
Jin Won
JW
D000818:Animals; D017209:Apoptosis / Q000187:drug effects / Q000528:radiation effects; D002460:Cell Line; D002470:Cell Survival / Q000187:drug effects / Q000528:radiation effects; D006224:Cricetinae; D003412:Cricetulus; D004249:DNA Damage / Q000187:drug effects / Q000528:radiation effects; D004147:Dioxins / Q000494:pharmacology*; D005347:Fibroblasts / Q000187:drug effects / Q000528:radiation effects; D016166:Free Radical Scavengers / Q000494:pharmacology; D005720:Gamma Rays / Q000009:adverse effects*; D048031:JNK Mitogen-Activated Protein Kinases / Q000378:metabolism; D008168:Lung / Q000166:cytology / Q000187:drug effects / Q000528:radiation effects; D048670:MAP Kinase Kinase 4 / Q000187:drug effects / Q000528:radiation effects; D018384:Oxidative Stress / Q000187:drug effects* / Q000528:radiation effects; D017382:Reactive Oxygen Species / Q000378:metabolism*; D018808:Transcription Factor AP-1 / Q000187:drug effects / Q000528:radiation effects
D004147:Dioxins; D016166:Free Radical Scavengers; D017382:Reactive Oxygen Species; D018808:Transcription Factor AP-1; C060311:eckol; D048031:JNK Mitogen-Activated Protein Kinases; D048670:MAP Kinase Kinase 4