Document Detail


Effects of EGCG on voltage-gated sodium channels in primary cultures of rat hippocampal CA1 neurons.
MedLine Citation:
PMID:  18706964     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
(-)-Epigallocatechin-3-gallate (EGCG), the main active component of green tea, is commonly known for its beneficial properties at low doses. On the other hand, little is known about the adverse effects of EGCG. Voltage-gated sodium channel (VGSC) is responsible for both initiation and propagation of action potentials of the neurons in the hippocampus and throughout the central nervous system (CNS). In this study, the effects of EGCG on voltage-gated sodium channel currents (I(Na)) were investigated in rat primary cultures of hippocampal CA1 neurons via the conventional whole-cell patch-clamp technique. We found that I(Na) was not affected by EGCG at the concentration of 0.1microM, but was completely blocked by EGCG at the concentration of 400microM and higher, and EGCG reduced the amplitudes of I(Na) in a concentration-dependent manner in the range of 0.1-400microM. Furthermore, our results also showed that at the concentration of 100microM, EGCG was known to have the following performances: (1) it decreased the activation threshold and the voltage at which the maximum I(Na) current was evoked, caused negative shifts of I(Na) steady-state activation curve. (2) It enlarged I(Na) tail-currents. (3) It induced a left shift of the steady-state inactivation. (4) It reduced fraction of available sodium channels. (5) It delayed the activation of I(Na) in a voltage-dependent manner. (6) It prolonged the time course of the fast inactivation of sodium channels. (7) It accelerated the activity-dependent attenuation of I(Na). On the basis of these findings, we propose that EGCG could impair certain physiological functions of VGSCs, which may contribute, directly or indirectly, to EGCG's effects in CNS.
Authors:
Hong-Min Deng; Shu-Ting Yin; Dan Yan; Ming-Liang Tang; Chen-Chen Li; Ju-Tao Chen; Ming Wang; Di-Yun Ruan
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't     Date:  2008-07-29
Journal Detail:
Title:  Toxicology     Volume:  252     ISSN:  0300-483X     ISO Abbreviation:  Toxicology     Publication Date:  2008 Oct 
Date Detail:
Created Date:  2008-10-13     Completed Date:  2009-01-05     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  0361055     Medline TA:  Toxicology     Country:  Ireland    
Other Details:
Languages:  eng     Pagination:  1-8     Citation Subset:  IM    
Affiliation:
School of Life Science, University of Science and Technology of China, Hefei, Anhui 230027, PR China.
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MeSH Terms
Descriptor/Qualifier:
Animals
Animals, Newborn
Catechin / analogs & derivatives*,  pharmacology
Cells, Cultured
Data Interpretation, Statistical
Dose-Response Relationship, Drug
Electrophysiology
Hippocampus / cytology*,  drug effects
Ion Channel Gating / drug effects
Neurons / drug effects,  metabolism*
Patch-Clamp Techniques
Rats
Sodium Channel Blockers / pharmacology
Sodium Channels / agonists*,  metabolism
Chemical
Reg. No./Substance:
0/Sodium Channel Blockers; 0/Sodium Channels; 154-23-4/Catechin; 989-51-5/epigallocatechin gallate

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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