Chronic green tea catechins administration prevents oxidative stress-related brain aging in C57BL/6J mice

Brain Res. 2010 Sep 24;1353:28-35. doi: 10.1016/j.brainres.2010.07.074. Epub 2010 Aug 1.


As the organism ages, production of reactive oxygen species (ROS) increases while antioxidants defense capability declines, leading to oxidative stress in critical cellular components, which further enhances ROS production. In the brain, this vicious cycle is more severe as brain is particularly vulnerable to oxidative damage. In our study, 14-month-old female C57BL/6J mice were orally administered 0.05% green tea catechins (GTC, w/v) in drinking water for 6 months. We found that GTC supplementation prevented the decrease in total superoxide dismutase and glutathione peroxidase activities in serum as well as reduced the thiobarbituric acid reactive substances and protein carbonyl contents in the hippocampus of aged mice. The activation of transcriptional factor nuclear factor-kappa B and lipofuscin formation in pyramidal cells of hippocampal CA1 region, which are all related to oxidative stress, was also reduced after GTC treatment. We also found that long-term GTC treatment prevented age-related reductions of two representative post-synaptic proteins post-synaptic density 95 and N-methyl-d-aspartate receptor 1 in the hippocampus. These results demonstrated that chronic 0.05% green tea catechins administration may prevent oxidative stress related brain aging in female C57BL/6J mice.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Age Factors
  • Aging* / drug effects
  • Animals
  • Antioxidants / administration & dosage*
  • Body Weight / drug effects
  • Catechin / administration & dosage*
  • Cerebral Cortex / cytology
  • Cerebral Cortex / drug effects
  • Disks Large Homolog 4 Protein
  • Female
  • GAP-43 Protein / metabolism
  • Glutathione Peroxidase / blood
  • Guanylate Kinases
  • Hippocampus / cytology
  • Hippocampus / drug effects*
  • Intracellular Signaling Peptides and Proteins / metabolism
  • Membrane Proteins / metabolism
  • Mice
  • Mice, Inbred C57BL
  • NF-kappa B / metabolism
  • Oxidative Stress / drug effects*
  • Protein Carbonylation / drug effects
  • Random Allocation
  • Receptors, N-Methyl-D-Aspartate / metabolism
  • Superoxide Dismutase / metabolism
  • Synaptophysin / metabolism
  • Thiobarbituric Acid Reactive Substances / metabolism


  • Antioxidants
  • Disks Large Homolog 4 Protein
  • Dlg4 protein, mouse
  • GAP-43 Protein
  • Intracellular Signaling Peptides and Proteins
  • Membrane Proteins
  • NF-kappa B
  • NMDA receptor A1
  • Receptors, N-Methyl-D-Aspartate
  • Synaptophysin
  • Thiobarbituric Acid Reactive Substances
  • Catechin
  • Glutathione Peroxidase
  • Superoxide Dismutase
  • Guanylate Kinases