1. Protective effects of Korean red ginseng against radiation-induced apoptosis in human HaCaT keratinocytes.
- Author
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Chang JW, Park KH, Hwang HS, Shin YS, Oh YT, and Kim CH
- Subjects
- Apoptosis drug effects, Apoptosis physiology, Apoptosis radiation effects, Cell Line, Cell Movement drug effects, Cell Movement physiology, Cell Movement radiation effects, Cell Proliferation drug effects, Cell Proliferation physiology, Cell Proliferation radiation effects, Cell Survival drug effects, Cell Survival physiology, Cell Survival radiation effects, Dose-Response Relationship, Drug, Dose-Response Relationship, Radiation, Humans, Keratinocytes cytology, Korea, Oxidative Stress drug effects, Oxidative Stress physiology, Oxidative Stress radiation effects, Radiation Tolerance drug effects, Keratinocytes physiology, Keratinocytes radiation effects, Panax chemistry, Plant Extracts administration & dosage, Radiation Tolerance physiology, Radiation-Protective Agents administration & dosage, Reactive Oxygen Species metabolism
- Abstract
Radiation-induced oral mucositis is a dose-limiting toxic side effect for patients with head and neck cancer. Numerous attempts at improving radiation-induced oral mucositis have not produced a qualified treatment. Ginseng polysaccharide has multiple immunoprotective effects. Our aim was to investigate the effectiveness of Korean red ginseng (KRG) on radiation-induced damage in the human keratinocyte cell line HaCaT and in an in vivo zebrafish model. Radiation inhibited HaCaT cell proliferation and migration in a cell viability assay and wound healing assay, respectively. KRG protected against these effects. KRG attenuated the radiation-induced embryotoxicity in the zebrafish model. Irradiation of HaCaT cells caused apoptosis and changes in mitochondrial membrane potential (MMP). KRG inhibited the radiation-induced apoptosis and intracellular generation of reactive oxygen species (ROS), and stabilized the radiation-induced loss of MMP. Western blots revealed KRG-mediated reduced expression of ataxia telangiectasia mutated protein (ATM), p53, c-Jun N-terminal kinase (JNK), p38 and cleaved caspase-3, compared with their significant increase after radiation treatment. The collective results suggest that KRG protects HaCaT cells by blocking ROS generation, inhibiting changes in MMP, and inhibiting the caspase, ATM, p38 and JNK pathways.
- Published
- 2014
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