Preventive Nutrition and Food Science

  • 제19권4호
  • /
  • Pages.348-352
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  • 2014
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  • 2287-1098(pISSN)
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  • 2287-8602(eISSN)
한국식품영양과학회 (The Korean Society of Food Science and Nutrition)
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Protective Effects of Black Rice Extracts on Oxidative Stress Induced by tert-Butyl Hydroperoxide in HepG2 Cells

  • Lee, Seon-Mi (Department of Food Science and Biotechnology, Chungbuk National University) ;
  • Choi, Youngmin (Functional Food & Nutrition Division, Department of AgroFood Resources, Rural Development Administration) ;
  • Sung, Jeehye (Department of Food Science and Biotechnology, Chungbuk National University) ;
  • Kim, Younghwa (Department of Food Science and Biotechnology, Chungbuk National University) ;
  • Jeong, Heon-Sang (Department of Food Science and Biotechnology, Chungbuk National University) ;
  • Lee, Junsoo (Department of Food Science and Biotechnology, Chungbuk National University)
  • 투고 : 2014.07.31
  • 심사 : 2014.10.31
  • 발행 : 2014.12.31
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초록

Black rice contains many biologically active compounds. The aim of this study was to investigate the protective effects of black rice extracts (whole grain extract, WGE and rice bran extract, RBE) on tert-butyl hydroperoxide (TBHP)-induced oxidative injury in HepG2 cells. Cellular reactive oxygen species (ROS), antioxidant enzyme activities, malondialdehyde (MDA) and glutathione (GSH) concentrations were evaluated as biomarkers of cellular oxidative status. Cells pretreated with 50 and $100{\mu}g/mL$ of WGE or RBE were more resistant to oxidative stress in a dose-dependent manner. The highest WGE and BRE concentrations enhanced GSH concentrations and modulated antioxidant enzyme activities (glutathione reductase, glutathione-S-transferase, catalase, and superoxide dismutase) compared to TBHP-treated cells. Cells treated with RBE showed higher protective effect compared to cells treated with WGE against oxidative insult. Black rice extracts attenuated oxidative insult by inhibiting cellular ROS and MDA increase and by modulating antioxidant enzyme activities in HepG2 cells.

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