Home >> Clinical and Experimental Pharmacology and Physiology, Volume 31, Number 8

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

Authors: Jong-Hun Lee; Dae-Kyu Song; Chul-Ho Jung1; Dong-Hoon Shin2; JongWook Park2; Taeg Kyu Kwon2; Byeong-Churl Jang2; Kyo-Cheol Mun2; Sang-Pyo Kim2; Seong-Il Suh2; Jae Hoon Bae

Source: Clinical and Experimental Pharmacology and Physiology, Volume 31, Number 8, August 2004 , pp. 530-536(7)

Publisher: Wiley-Blackwell

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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 dose-dependent manner. (–)-Epigallocatechin gallate attenuated this glutamate (30 mmol/L)-induced [Ca2+]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 Ca2+ influx, but not metabotropic receptor-mediated Ca2+ release.

4. These results suggest that EGCG reduces the glutamate-induced [Ca2+]i increase by attenuating ionotropic Ca2+ influx and that this promotes the viability of PC12 cells.

Keywords: (–)-epigallocatechin gallate; glutamate; intracellular calcium modulation

Document Type: Research article

DOI: http://dx.doi.org/10.1111/j.1440-1681.2004.04044.x

Affiliations: 1: Psychiatry, and 2: Chronic Disease Research Center, Keimyung University, Daegu, South Korea

Publication date: 2004-08-01

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