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Neuroprotective Effect of L-Theanine on Aβ-Induced Neurotoxicity through Anti-Oxidative Mechanisms in SK-N-SH and SK-N-MC Cells

  • Jo, Mi-Ran (College of Pharmacy and Medical Research Center, Chungbuk National University) ;
  • Park, Mi-Hee (College of Pharmacy and Medical Research Center, Chungbuk National University) ;
  • Choi, Dong-Young (College of Pharmacy and Medical Research Center, Chungbuk National University) ;
  • Yuk, Dong-Yeun (College of Pharmacy and Medical Research Center, Chungbuk National University) ;
  • Lee, Yuk-Mo (College of Pharmacy and Medical Research Center, Chungbuk National University) ;
  • Lee, Jin-Moo (College of Pharmacy and Medical Research Center, Chungbuk National University) ;
  • Jeong, Jae-Hwang (Department of Biotechnology and Bioinformatics, Chungbuk Provincial College of Science & Technology) ;
  • Oh, Ki-Wan (College of Pharmacy and Medical Research Center, Chungbuk National University) ;
  • Lee, Moon-Soon (College of Chungbuk National University) ;
  • Han, Sang-Bae (College of Pharmacy and Medical Research Center, Chungbuk National University) ;
  • Hong, Jin-Tae (College of Pharmacy and Medical Research Center, Chungbuk National University)
  • Received : 2011.03.31
  • Accepted : 2011.05.19
  • Published : 2011.07.31

Abstract

Amyloid beta ($A{\beta}$)-induced neurotoxicity is a major pathological mechanism of Alzheimer's disease (AD). In this study, we investigated the inhibitory effect of L-theanine, a component of green tea (Camellia sinensis) on $A{\beta}_{1-42}$-induced neurotoxicity and oxidative damages of macromolecules. L-theanine inhibited $A{\beta}_{1-42}$-induced generation of reactive oxygen species, and activation of extracellular signal-regulated kinase and p38 mitogenic activated protein kinase as well as the activity of nuclear factor kappa-B. L-theanine also signifi cantly reduced oxidative protein and lipid damage, and elevated glutathione level. Consistent with the reduced neurotoxic signals, L-theanine (10-50 ${\mu}g$/ml) concomitantly attenuated $A{\beta}_{1-42}$ (5 ${\mu}M$)-induced neurotoxicity in SK-N-MC and SK-N-SH human neuroblastoma cells. These data indicate that L-theanine on $A{\beta}$-induced neurotoxicity prevented oxidative damages of neuronal cells, and may be useful in the prevention and treatment of neurodegenerative disease like AD.

Keywords

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