Protective effect of (-)-epigallocatechin gallate against advanced glycation endproducts-induced injury in neuronal cells

Sun Joo Lee, Kwang Won Lee

Research output: Contribution to journalArticlepeer-review

62 Citations (Scopus)


Advanced glycation endproducts (AGEs) are believed to be secondary factors in the selective neuronal injury associated with several neurodegenerative disorders. In this study, we investigated the protective effects of (-)-epigallocatechin gallate (EGCG), a major monomer of green tea polyphenols, against AGEs-induced damage in neuron cells. The results showed that EGCG treatment protected against glyceraldehyde-derived AGE-induced neurotoxicity, which is associated with an increase in intracellular reactive oxygen species, as well as against decreases in intracellular catalase (CAT) and superoxide dismutase (SOD) activities. EGCG treatment also decreased malondialdehyde and carbonyl levels, and AGEs formation. Treatment with 10 μM EGCG upregulated SOD and CAT levels, whereas glutathione peroxidase activity was reduced. Furthermore, 5 μM EGCG was found to down-regulate the mRNA level of the AGE receptor (RAGE) in neuronal cells up to 2.5 fold, as determined by real time PCR. The results demonstrated that EGCG may exhibit protective effects against AGEs-induced injury in neuronal cells through its antioxidative properties, as well as by interfering with AGEs-RAGE interaction mediated pathways, suggesting a beneficial role for this tea catechin against neurodegenerative diseases.

Original languageEnglish
Pages (from-to)1369-1373
Number of pages5
JournalBiological and Pharmaceutical Bulletin
Issue number8
Publication statusPublished - 2007 Aug


  • (-)-epigallocatechin gallate
  • Advanced glycation endproduct
  • Alzheimer's disease
  • Apoptosis
  • Free radical

ASJC Scopus subject areas

  • Pharmacology
  • Pharmaceutical Science


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