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(–)‐EPIGALLOCATECHIN GALLATE ATTENUATES GLUTAMATE‐INDUCED CYTOTOXICITY VIA INTRACELLULAR CA 2+ MODULATION IN PC12 CELLS
Author(s) -
Lee JongHun,
Song DaeKyu,
Jung ChulHo,
Shin DongHoon,
Park JongWook,
Kwon Taeg Kyu,
Jang ByeongChurl,
Mun KyoCheol,
Kim SangPyo,
Suh SeongIl,
Bae Jae Hoon
Publication year - 2004
Publication title -
clinical and experimental pharmacology and physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.752
H-Index - 103
eISSN - 1440-1681
pISSN - 0305-1870
DOI - 10.1111/j.1440-1681.2004.04044.x
Subject(s) - glutamate receptor , cytotoxicity , chemistry , epigallocatechin gallate , ionotropic effect , intracellular , viability assay , calcium , biochemistry , calcium in biology , kainate receptor , pharmacology , biophysics , microbiology and biotechnology , receptor , polyphenol , biology , cell , antioxidant , in vitro , ampa receptor , organic chemistry
SUMMARY 1. The effects of (–)‐epigallocatechin gallate (EGCG), a green tea polyphenol, on glutamate‐induced increases in intracellular Ca 2+ concentrations ([Ca 2+ ] i ) and cytotoxicity in PC12 cells were investigated. 2. Changes in [Ca 2+ ] i were measured using Fura‐2/AM calcium indicator dye and cellular viabilities were determined by a viable cell count and a 3‐(4,4‐dimethylthiazol‐2‐yl)‐2,5‐diphenyltetrazolium bromide reduction assay. 3. Glutamate increased [Ca 2+ ] i in PC12 cells in a dose‐dependent manner. (–)‐Epigallocatechin gallate attenuated this glutamate (30 mmol/L)‐induced [Ca 2+ ] i increase and EGCG (50 µmol/L) increased the viability of PC12 cells against glutamate‐induced cytotoxicity. The EGCG effect was also found to be independent of its general anti‐oxidant mechanism. In contrast, EGCG directly suppressed both N ‐methyl‐ d ‐aspartate (50 mmol/L)‐ and kainate (20 mmol/L)‐mediated Ca 2+ influx, but not metabotropic receptor‐mediated Ca 2+ release. 4. These results suggest that EGCG reduces the glutamate‐induced [Ca 2+ ] i increase by attenuating ionotropic Ca 2+ influx and that this promotes the viability of PC12 cells.