期刊
EUROPEAN JOURNAL OF PHARMACOLOGY
卷 591, 期 1-3, 页码 114-123出版社
ELSEVIER SCIENCE BV
DOI: 10.1016/j.ejphar.2008.06.086
关键词
eckol; radiation; oxidative stress; reactive oxygen species; apoptosis; JNK pathway
资金
- Ministry of Science & Technology of Korea (KOSEF) [M1063901]
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 NH2-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. (C) 2008 Elsevier B.V. All rights reserved.
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