Cellular targets for the beneficial actions of tea polyphenols1234

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ABSTRACT

Green and black teas contain different biologically active polyphenolic compounds that might offer protection against a variety of human diseases. Although promising experimental and clinical data have shown protective effects, limited information is available on how these beneficial effects of tea polyphenols are mediated at the cellular level. Evidence is accumulating that catechins in green tea as well as theaflavins and thearubigins from black tea are the substances responsible for the physiologic effects of tea in vitro. The green tea catechin epigallocatechin-3-gallate (EGCG) is generally considered to be the biologically most active compound in vitro. The changes in the activities of various protein kinases, growth factors, and transcription factors represent a common mechanism involved in cellular effects of tea polyphenols. In addition to modification of intracellular signaling by activation of cellular receptors, it was shown that, at least for EGCG, tea polyphenols can enter the cells and directly interact with their molecular targets within cells. There, they frequently result in opposite effects in primary compared with tumor cells. Although tea polyphenols were long regarded as antioxidants, research in recent years has uncovered their prooxidant properties. The use of high nonphysiologic concentrations in many cell culture studies raises questions about the biological relevance of the observed effects for the in vivo situation. Efforts to attribute functional effects in vivo to specific molecular targets at the cellular level are still ongoing.

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1

From Charité–Universitätsmedizin Berlin, Medizinische Klinik für Kardiologie und Angiologie, CCM, Berlin, Germany.

2

Presented at the conference “Fifth International Scientific Symposium on Tea and Human Health,” held at the US Department of Agriculture, Washington, DC, 19 September 2012. The conference was organized by Jeffrey Blumberg, Tufts University, Boston, MA, and a Steering Committee including representatives from each of the symposium cosponsors: the American Cancer Society, the American College of Nutrition, the American Institute for Cancer Research, the American Medical Women’s Association, the American Society for Nutrition, and the Linus Pauling Institute. The symposium was underwritten by the Tea Council of the USA. Its contents are solely the responsibility of the authors and do not necessarily represent the official views of the Tea Council of the USA or the cosponsoring organizations.

3

ML received an honorarium and travel support from the Tea Council of the USA for speaking at the Fifth International Scientific Symposium on Tea and Human Health and for preparing this article for publication.

4

Address correspondence to M Lorenz, Charité–Universitätsmedizin Berlin, Medizinische Klinik für Kardiologie und Angiologie, Campus Mitte, Kardiologisches Forschungslabor, Hessische Straße 3-4, 10115 Berlin, Germany. E-mail: [email protected].

5

Abbreviations used: EGCG, epigallocatechin-3-gallate; eNOS, endothelial nitric oxide synthase; ERα, estrogen receptor α; FITC, fluorescein isothiocyanate; miRNA, microRNA; mRNA, messenger RNA; NO, nitric oxide; ROS, reactive oxygen species; TF3, theaflavin-3,3′-digallate; 67LR, 67-kDa laminin receptor.