HOMEPRODUCTSCOMPANYCONTACTFAQResearchDictionaryPharmaSign Up FREE or Login

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

Abstract
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+] ([Ca2+]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 micro M) also significantly inhibited the EGCG-induced [Ca2+]i increases. Treatment for 15 min with the phospholipase C (PLC) inhibitor neomycin (300 micro M) attenuated the increases significantly, while the tyrosine kinase inhibitor genistein (30 micro M) had no effect. EGCG increased [3H]-inositol phosphates formation via PLC activation. Treatment for 10 min with mefenamic acid (100 micro M) and flufenamic acid (100 micro M), derivatives of diphenylamine-2-carboxylate, blocked the EGCG-induced [Ca2+]i increase in non-treated and thapsigargin-treated cells but indomethacin (100 micro M) did not affect the increases. Collectively, these data suggest that EGCG increases [Ca2+]i 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.
AuthorsHee 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
JournalNaunyn-Schmiedeberg's archives of pharmacology (Naunyn Schmiedebergs Arch Pharmacol) Vol. 369 Issue 2 Pg. 260-7 (Feb 2004) ISSN: 0028-1298 [Print] Germany
PMID14647974 (Publication Type: Comparative Study, Journal Article, Research Support, Non-U.S. Gov't)
Chemical References
  • Inositol Phosphates
  • Ion Channels
  • Tea
  • ortho-Aminobenzoates
  • Mefenamic Acid
  • Flufenamic Acid
  • Catechin
  • fenamic acid
  • epigallocatechin gallate
  • Genistein
  • Protein-Tyrosine Kinases
  • Type C Phospholipases
  • Calcium
Topics
  • Calcium (metabolism)
  • Catechin (analogs & derivatives, pharmacology)
  • Enzyme Activation
  • Flufenamic Acid (chemistry, pharmacology)
  • Genistein (pharmacology)
  • Inositol Phosphates (biosynthesis)
  • Ion Channels (antagonists & inhibitors)
  • Mefenamic Acid (chemistry, pharmacology)
  • Protein-Tyrosine Kinases (antagonists & inhibitors)
  • Tea (chemistry)
  • Tumor Cells, Cultured
  • Type C Phospholipases (antagonists & inhibitors, metabolism)
  • ortho-Aminobenzoates (chemistry)

Join CureHunter, for free Research Interface BASIC access!

Take advantage of free CureHunter research engine access to explore the best drug and treatment options for any disease. Find out why thousands of doctors, pharma researchers and patient activists around the world use CureHunter every day.
Realize the full power of the drug-disease research graph!


Choose Username:
Email:
Password:
Verify Password:
Enter Code Shown: