Inhibitiory effect of green tea extract on $A\beta$-induced PC12 cell death

  • Lee, Sun-Young (College of Pharmacy, Chungbuk National University) ;
  • Lee, Seung-Ho (Soonchunhyang University, Department Food Science and Nutrition, and Korea Food Research Institut) ;
  • Son, Dong-Ju (Soonchunhyang University, Department Food Science and Nutrition, and Korea Food Research Institut) ;
  • Kim, Su-Jin (Soonchunhyang University, Department Food Science and Nutrition, and Korea Food Research Institut) ;
  • Ha, Tae-Youl (Soonchunhyang University, Department Food Science and Nutrition, and Korea Food Research Institut) ;
  • Yun, Yeo-Pyo (Soonchunhyang University, Department Food Science and Nutrition, and Korea Food Research Institut) ;
  • Oh, Ki-Wan (Soonchunhyang University, Department Food Science and Nutrition, and Korea Food Research Institut) ;
  • Hong, Jin-Tae (Soonchunhyang University, Department Food Science and Nutrition, and Korea Food Research Institute)
  • Published : 2003.10.01

Abstract

Beta-amyloid peptide (A${\beta}$) is considered to be responsible for the pathogenesis of the Alzheimer's disease. Several lines of evidence support that A${\beta}$-amyloid-induced cytotoxicity is mediated through the generation of reactive oxygen species (ROS). Agents that are able to scavenge excess ROS may be useful as protecting or reducing agents for development or progress of AD. Green tea extract has been known to have antioxidant property. Our previous studies also demonstrate that green tea extract protected ischemia/reperfusion-induced brain injury by reduction of cell death through scavenging of oxidative damages of macromolecules. (omitted)

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