Abstract
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 language | English |
|---|---|
| Pages (from-to) | 1369-1373 |
| Number of pages | 5 |
| Journal | Biological and Pharmaceutical Bulletin |
| Volume | 30 |
| Issue number | 8 |
| DOIs | |
| Publication status | Published - 2007 Aug 1 |
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Keywords
- (-)-epigallocatechin gallate
- Advanced glycation endproduct
- Alzheimer's disease
- Apoptosis
- Free radical
ASJC Scopus subject areas
- Molecular Medicine
- Pharmacology, Toxicology and Pharmaceutics(all)
Cite this
Protective effect of (-)-epigallocatechin gallate against advanced glycation endproducts-induced injury in neuronal cells. / Lee, Sun J.; Lee, Kwang Won.
In: Biological and Pharmaceutical Bulletin, Vol. 30, No. 8, 01.08.2007, p. 1369-1373.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - Protective effect of (-)-epigallocatechin gallate against advanced glycation endproducts-induced injury in neuronal cells
AU - Lee, Sun J.
AU - Lee, Kwang Won
PY - 2007/8/1
Y1 - 2007/8/1
N2 - 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.
AB - 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.
KW - (-)-epigallocatechin gallate
KW - Advanced glycation endproduct
KW - Alzheimer's disease
KW - Apoptosis
KW - Free radical
UR - http://www.scopus.com/inward/record.url?scp=34548027316&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=34548027316&partnerID=8YFLogxK
U2 - 10.1248/bpb.30.1369
DO - 10.1248/bpb.30.1369
M3 - Article
C2 - 17666787
AN - SCOPUS:34548027316
VL - 30
SP - 1369
EP - 1373
JO - Biological and Pharmaceutical Bulletin
JF - Biological and Pharmaceutical Bulletin
SN - 0918-6158
IS - 8
ER -