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(–)-EPIGALLOCATECHIN GALLATE ATTENUATES GLUTAMATE-INDUCED CYTOTOXICITY VIA INTRACELLULAR CA2+ MODULATION IN PC12 CELLS

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Affiliated Author(s)
정철호송대규배재훈권택규박종욱서성일김상표문교철장병철신동훈
Alternative Author(s)
Jung, Chul HoSong, Dae KyuBae, Jae HoonKwon, Taeg KyuPark, Jong WookSuh, Seong IlKim, Sang PyoMun, Kyo CheolJang, Byeong ChurlShin, Dong Hoon
Journal Title
Clinical and Experimental Pharmacology and Physiology
ISSN
0305-1870
Issued Date
2004
Abstract
SUMMARY
1. The effects of (–)-epigallocatechin gallate (EGCG), a
green tea polyphenol, on glutamate-induced increases in intracellular
Ca2+ concentrations ([Ca2+]i) and cytotoxicity in PC12
cells were investigated.
2. Changes in [Ca2+]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 [Ca2+]i in PC12 cells in a dosedependent
manner. (–)-Epigallocatechin gallate attenuated this
glutamate (30 mmol/L)-induced [Ca2+]i increase and EGCG
(50
mol/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-Daspartate
(50 mmol/L)- and kainate (20 mmol/L)-mediated
Ca2+ influx, but not metabotropic receptor-mediated Ca2+
release.
4. These results suggest that EGCG reduces the glutamateinduced
[Ca2+]i increase by attenuating ionotropic Ca2+ influx
and that this promotes the viability of PC12 cells.
Key words: (–)-epigallocatechin gallate, glutamate, intracellular
calcium modulation.
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