Epigallocatechin-3-gallate increases intracellular [Ca2+] in U87 cells mainly by influx of extracellular Ca2+ and partly by release of intracellular stores

Hee Jung Kim, Keun Sang Yum, Jong Ho Sung, Duck Joo Rhie, Myung Jun Kim, Do Sik Min, Sang June Hahn, Myung Suk Kim, Yang Hyeok Jo, Shin Hee Yoon

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33 Citations (Scopus)


Green tea has been receiving considerable attention as a possible preventive agent against cancer and cardiovascular disease. Epigallocatechin-3- gallate (EGCG) is a major polyphenol component of green tea. Using digital calcium imaging and an assay for [3H]-inositol phosphates, we determined whether EGCG increases intracellular [Ca2+] ([Ca 2+]i) in non-excitable human astrocytoma U87 cells. EGCG induced concentration-dependent increases in [Ca2+]i. The EGCG-induced [Ca2+]i increases were reduced to 20.9% of control by removal of extracellular Ca2+. The increases were also inhibited markedly by treatment with the non-specific Ca2+ channel inhibitors cobalt (3 mM) for 3 min and lanthanum (1 mM) for 5 min. The increases were not significantly inhibited by treatment for 10 min with the L-type Ca2+ channel blocker nifedipine (100 nM). Treatment with the inhibitor of endoplasmic reticulum Ca2+-ATPase thapsigargin (1 μM) also significantly inhibited the EGCG-induced [Ca2+]i increases. Treatment for 15 min with the phospholipase C (PLC) inhibitor neomycin (300 μM) attenuated the increases significantly, while the tyrosine kinase inhibitor genistein (30 μM) had no effect. EGCG increased [ 3H]-inositol phosphates formation via PLC activation. Treatment for 10 min with mefenamic acid (100 μM) and flufenamic acid (100 μM), derivatives of diphenylamine-2-carboxylate, blocked the EGCG-induced [Ca 2+]i increase in non-treated and thapsigargin-treated cells but indomethacin (100 μM) did not affect the increases. Collectively, these data suggest that EGCG increases [Ca2+]; in non-excitable U87 cells mainly by eliciting influx of extracellular Ca2+ and partly by mobilizing intracellular Ca2+ stores by PLC activation. The EGCG-induced [Ca2+]i influx is mediated mainly through channels sensitive to diphenylamine-2-carboxylate derivatives.

Original languageEnglish
Pages (from-to)260-267
Number of pages8
JournalNaunyn-Schmiedeberg's Archives of Pharmacology
Issue number2
Publication statusPublished - 2004 Feb

Bibliographical note

Funding Information:
Acknowledgements This work was supported by grant No. R01-1999-000-00107-0 from the Basic Research Program of the Korea Science and Engineering Foundation and the Roche Foundation made in the program year 2000.

All Science Journal Classification (ASJC) codes

  • Pharmacology


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