Epigallocatechin-3-gallate induced primary cultures of rat hippocampal neurons death linked to calcium overload and oxidative stress
| Autor: | Tairan Xing, Ju-Tao Chen, Di-Yun Ruan, Mingliang Tang, Hui-Li Wang, Shu-Ting Yin, Hong-Min Deng |
|---|---|
| Rok vydání: | 2009 |
| Předmět: |
Programmed cell death
Antioxidant medicine.medical_treatment Oxidative phosphorylation Green tea extract Biology Hippocampal formation Pharmacology medicine.disease_cause Hippocampus complex mixtures Catechin Membrane Potentials medicine Animals heterocyclic compounds Rats Wistar Cells Cultured Neurons chemistry.chemical_classification Reactive oxygen species Cell Death Dose-Response Relationship Drug food and beverages General Medicine Rats Oxidative Stress chemistry Biochemistry Apoptosis Calcium sense organs Oxidative stress Signal Transduction |
| Zdroj: | Naunyn-Schmiedeberg's Archives of Pharmacology. 379:551-564 |
| ISSN: | 1432-1912 0028-1298 |
| DOI: | 10.1007/s00210-009-0401-4 |
| Popis: | Epigallocatechin-3-gallate (EGCG), a catechin polyphenols component, is the main ingredient of green tea extract. It has been reported that EGCG is a potent antioxidant and beneficial in oxidative stress-related diseases, but others and our previous study showed that EGCG has pro-oxidant effects at high concentration. Thus, in this study, we tried to examine the possible pathway of EGCG-induced cell death in cultures of rat hippocampal neurons. Our results showed that EGCG caused a rapid elevation of intracellular free calcium levels ([Ca2+]i) in a dose-dependent way. Exposure to EGCG dose- and time-dependently increased the production of reactive oxygen species (ROS) and reduced mitochondrial membrane potential (Δψ m) as well as the Bcl-2/Bax expression ratio. Importantly, acetoxymethyl ester of 5,5′-dimethyl-bis(o-aminophenoxy)ethane-N,N,N′,N′-tetraacetic acid, ethylene glycol-bis-(2-aminoethyl)-N,N,N′,N′-tetraacetic acid, and vitamin E could attenuate EGCG-induced apoptotic responses, including ROS generation, mitochondrial dysfunction, and finally partially prevented EGCG-induced cell death. Furthermore, treatment of hippocampal neurons with EGCG resulted in an elevation of caspase-3 and caspase-9 activities with no significant accompaniment of lactate dehydrogenase release, which provided further evidence that apoptosis was the dominant mode of EGCG-induced cell death in cultures of hippocampal neurons. Taken together, these findings indicated that EGCG induced hippocampal neuron death through the mitochondrion-dependent pathway. |
| Databáze: | OpenAIRE |
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