Protective effect of (-)-epigallocatechin gallate against advanced glycation endproducts-induced injury in neuronal cells.
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 muM EGCG upregulated SOD and CAT levels, whereas glutathione peroxidase activity was reduced. Furthermore, 5 muM 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.
Lee
Sun-joo
SJ
Department of Food Science, College of Life Sciences & Biotechnology, Korea University [corrected] 1,5 ga, Anam-dong, Sungbuk-ku, Seoul 136-701.
Lee
Kwang-Won
KW
D017304:Annexin A5 / Q000378:metabolism; D000975:Antioxidants / Q000378:metabolism; D017209:Apoptosis / Q000187:drug effects; D002374:Catalase / Q000378:metabolism; D002392:Catechin / Q000031:analogs & derivatives* / Q000494:pharmacology; D045744:Cell Line, Tumor; D002470:Cell Survival / Q000187:drug effects; D005979:Glutathione Peroxidase / Q000378:metabolism; D017127:Glycation End Products, Advanced / Q000037:antagonists & inhibitors* / Q000633:toxicity*; D006801:Humans; D007202:Indicators and Reagents; D015227:Lipid Peroxidation / Q000187:drug effects; D008315:Malondialdehyde / Q000378:metabolism; D009447:Neuroblastoma; D009474:Neurons / Q000187:drug effects* / Q000473:pathology; D018696:Neuroprotective Agents / Q000494:pharmacology*; D018384:Oxidative Stress / Q000187:drug effects; D017382:Reactive Oxygen Species / Q000378:metabolism; D020133:Reverse Transcriptase Polymerase Chain Reaction; D015398:Signal Transduction / Q000187:drug effects; D013482:Superoxide Dismutase / Q000378:metabolism
D017304:Annexin A5; D000975:Antioxidants; D017127:Glycation End Products, Advanced; D007202:Indicators and Reagents; D018696:Neuroprotective Agents; D017382:Reactive Oxygen Species; D008315:Malondialdehyde; D002392:Catechin; C045651:epigallocatechin gallate; D002374:Catalase; D005979:Glutathione Peroxidase; D013482:Superoxide Dismutase