방사선 돌연변이 블랙베리 주성분 Cyanidin-3-glucoside의 과산화수소 유발 산화적 손상에 대한 세포 보호 효과

Protective Effect of Cyanidin-3-glucoside, the Major Component of Rubus fruticosus L. Mutants by Irradiation, on H2O2-induced Oxidative Damage in HepG2 Cells

  • 조병옥 (한국원자력연구원 첨단방사선연구소) ;
  • 소양강 (한국원자력연구원 첨단방사선연구소) ;
  • 이창욱 (한국원자력연구원 첨단방사선연구소) ;
  • 진창현 (한국원자력연구원 첨단방사선연구소) ;
  • 육홍선 (충남대학교 식품영양학과) ;
  • 정일윤 (한국원자력연구원 첨단방사선연구소)
  • Cho, Byoung Ok (Advanced Radiation Technology Institute, Korea Atomic Energy Research Institute) ;
  • So, Yangkang (Advanced Radiation Technology Institute, Korea Atomic Energy Research Institute) ;
  • Lee, Chang Wook (Advanced Radiation Technology Institute, Korea Atomic Energy Research Institute) ;
  • Jin, Chang Hyun (Advanced Radiation Technology Institute, Korea Atomic Energy Research Institute) ;
  • Yook, Hong Sun (Department of Food Science and Human Nutrition, Chungnam National University) ;
  • Jeong, Il Yun (Advanced Radiation Technology Institute, Korea Atomic Energy Research Institute)
  • 투고 : 2014.05.02
  • 심사 : 2014.05.29
  • 발행 : 2014.05.31

초록

This study was conducted to analyze the protective capacity of cyanidin-3-glucoside (C3G), which is rich in mulberry and blackberry as an anthocyanin pigment. In this study, we found that treatment with C3G significantly reduced ROS production in hydrogen peroxide $(H_2O_2)-treated$ HepG2 cells in a dose-dependent manner. In addition, treatment with C3G significantly increased the cell viability in a dose-dependent manner in $H_2O_2-treated$ HepG2 cells. Moreover, treatment with C3G dose-dependently decreased the release of LDH and activation of caspase-3 in HepG2 cells treated with $H_2O_2$. Furthermore, the DNA damage in $H_2O_2-treated$ HepG2 cells was decreased by C3G treatment when compared with the control group in a dose-dependent manner. Additionally, treatment with C3G recovered the activity of antioxidant enzymes such as superoxide dismutase and catalase in $H_2O_2-treated$ HepG2 cells. To summarize, these results suggest that C3G protects cells from $H_2O_2-induced$ oxidative damage by activating antioxidant enzymes.

키워드

과제정보

연구 과제 주관 기관 : 미래창조과학부