4.3 Article

Protective effects of Korean red ginseng against radiation-induced apoptosis in human HaCaT keratinocytes

Journal

JOURNAL OF RADIATION RESEARCH
Volume 55, Issue 2, Pages 245-256

Publisher

OXFORD UNIV PRESS
DOI: 10.1093/jrr/rrt109

Keywords

Korean red ginseng (KRG); head and neck cancer; radiation-induced mucositis; apoptosis; radioprotection

Funding

  1. National Research Foundation of Korea (NRF)
  2. Korean Government (MEST) [2010-0012821]
  3. Korean Society of Gingseng by the Korean Ginseng Corporation
  4. National Research Foundation of Korea [2010-0012821] Funding Source: Korea Institute of Science & Technology Information (KISTI), National Science & Technology Information Service (NTIS)

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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.

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