Empetrum nigrum var. japonicum Extract Suppresses γ-Ray Radiation-Induced Cell Damage via Inhibition of Oxidative Stress

被引:11
作者
Kim, Ki Cheon [1 ]
Lee, In Kyung [2 ,3 ]
Kang, Kyoung Ah [1 ]
Kim, Bum Joon [2 ,3 ,4 ]
Kim, Daeshin
Moon, Ji Young [5 ]
Yoo, Byoung Sam [5 ]
Hyun, Jin Won [1 ,1 ]
机构
[1] Cheju Natl Univ, Appl Radiol Sci Res Inst, Jejudaehakro 690756, Jeju, South Korea
[2] Seoul Natl Univ, Coll Med, Dept Microbiol, Seoul 110799, South Korea
[3] Seoul Natl Univ, Coll Med, Canc Res Inst, Seoul 110799, South Korea
[4] Halla Arboretum, Jeju City 110799, Jeju, South Korea
[5] COSMAX Inc, Cosmet R&D Ctr, Hwa Sung 445746, Gyeonggi, South Korea
来源
AMERICAN JOURNAL OF CHINESE MEDICINE | 2011年 / 39卷 / 01期
关键词
Empetrum nigrum var. japonicum; gamma-Ray Radiation; Reactive Oxygen Species; Antioxidant Enzymes; Apoptosis; INDUCED APOPTOSIS; GLUTATHIONE-PEROXIDASE; SUPEROXIDE-DISMUTASE; MEDIATED APOPTOSIS; PROTEIN; ASSAY; PATHWAY; FAMILY; RATS;
D O I
10.1142/S0192415X11008725
中图分类号
R [医药、卫生];
学科分类号
10 ;
摘要
The ethylacetate fraction of Empetrum nigrum var. japonicum (ENE) was shown to reduce intracellular reactive oxygen species (ROS) generated by gamma-radiation and activate antioxidant enzymes, such as superoxide dismutase (SOD), catalase (CAT), and gluthathion peroxidase (GPx). ENE protected cells against radiation-induced cellular DNA damage, membrane lipid peroxidation, and protein modification, which are the main points of radiation-induced damage. In addition, ENE recovered cell viability by inhibiting apoptosis after cells were treated with radiation. ENE treatment also reduced gamma-radiation induced Bax, and caspase 9 and 3 expression in irradiated cells. However, irradiated cells with ENE recovered Bcl-2 expression, which was reduced by radiation. This anti-apoptotic effect of ENE was due to the inhibition of mitogen-activated protein kinase kinase-4 (MKK4/SEK1)-c-Jun NH2-terminal kinase (JNK) cascades induced by gamma-radiation. In summary, these results suggest that ENE protects cells against gamma-radiation-induced oxidative stress via the reduction of ROS and attenuation of apoptosis.
引用
收藏
页码:161 / 170
页数:10
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