Cardiovascular effects of tea polyphenols

Impact of tea and single tea substances on nitric oxide (NO) production and endothelial function

Die kardiovaskulären Effekte der Tee-Polyphenole

Project Leadership: Dr. rer. nat. Mario Lorenz

In this project the influence of tea polyphenols on endothelial function is investigated. Tea catechins, especially EGCG, for which beneficial cardiovascular effects have been previously shown, are the main focus of our work.

We could demonstrate that EGCG increases the NO production in endothelial cells and leads to NO-dependent vasorelaxation in isolated aortic rings. Activation of the endothelial nitric oxide synthase (eNOS) was mainly caused by phosphorylation of the enzyme through a PI3K-AKT/PKA-dependent pathway. Based on these results, we could subsequently show in a study with healthy human volunteers that endothelial function was improved 2 hours after consumption of tea as compared to control (water only). Green and black tea proved to be equally potent in improving endothelial function. In another in vitro study we identified the contribution of particular, isolated compounds of green and black tea on cardivascular beneficial effects in endothelial cells and aortic rings. Furthermore, we showed that EGCG prevented the cytokine-induced expression of the atherogenic adhesion molecule VCAM-1, and reduced adhesion of monocytes to human endothelial cells. Besides beneficial effects on NO production and vasorelaxation, a number of additional protective properties are attributed to tea polyphenols in the cardiovascular system. The above data demonstrate that our team has successfully analysed various physiological and molecular actions of tea polyphenols in the cardiovascular system.

To top

Tea polyphenol-mediated cardioprotection against oxidative stress

Project leadership: Dr. med. Henryk Dreger

Reactive oxygen species (ROS) such as hydrogen peroxide and superoxide anions are generated by a variety of physiological and pathological processes. Under physiological conditions, ROS are degraded by antioxidative enzymes, e.g. catalase, superoxide dismutase and heme oxygenase 1. Many pathological processes, e.g. ischemia/ reperfusion injury, are associated with supraphysiological levels of ROS which exceed the antioxidative capacity of cellular defense mechanisms. Consequently, high ROS concentrations cause oxidative stress and severely damage proteins, membranes, and DNA.

In a recent project, we analyzed the effect of the tea polyphenols EGCG and TF3 on cardiac myocytes in an in vitro model of oxidative stress. Both polyphenols conferred potent but short-lasting cardioprotection. Further experiments attributed this protective effect to the ability of EGCG and TF3 to directly scavenge ROS.

To top


Lorenz M, Stangl K, Stangl V. Vascular effects of tea are suppressed by soy milk. Atherosclerosis 2009, 206:31-32

Zimmermann BF, Papagiannopoulos M, Brachmann S, Lorenz M, Stangl V, Galensa R. A shortcut from plasma to chromatographic analysis: Straightforward and fast sample preparation for analysis of green tea catechins in human plasma. J Chromatogr B 2009; 877:823-826

Lorenz M, Urban J, Engelhardt U, Baumann G, Stangl K, Stangl V. Green and black tea are equally potent stimuli of NO production and vasodilation: new insights into tea ingredients involved. Basic Res. Cardiol. 2009; 104:100-110

Lorenz M, Hellige N, Rieder P, Kinkel HT, Trimpert C, Staudt A, Felix SB, Baumann G, Stangl K, Stangl V. Positive inotropic effects of epigallocatechin-3-gallate (EGCG) involve activation of Na+/H+ and Na+/Ca2+ exchangers. Eur. J. Heart Fail. 2008;10:439-445

Jochmann N, Lorenz M, Krosigk A, Martus P, Böhm V, Baumann G, Stangl K, Stangl V. The efficacy of black tea in ameliorating endothelial function is equivalent to that of green tea. Br. J. Nutr. 2008;99:863-868

Dreger H, Lorenz M, Kehrer A, Baumann G, Stangl K, Stangl V. Characteristics of catechin- and theaflavin-mediated cardioprotection. Exp. Biol. Med. (Maywood) 2008;233:427-433

Lorenz M, Jochmann N, von Krosigk A, Martus P, Baumann G, Stangl K, Stangl V. Addition of milk prevents vascular protective effects of tea. Eur. Heart J. 2007;28:219-223

Stangl V, Dreger H, Stangl K, Lorenz M. Molecular targets of tea polyphenols in the cardiovascular system. Cardiovasc. Res. 2007;73:348-358

Stangl V, Lorenz M, Stangl K. The role of tea and tea flavonoids in cardiovascular health. Mol. Nutr. Food Res. 2006;50:218-228

Lorenz M, Wessler S, Follmann E, Michaelis W, Dusterhoft T, Baumann G, Stangl K, Stangl V. A constituent of green tea, epigallocatechin-3-gallate, activates endothelial nitric oxide synthase by a phosphatidylinositol-3-OH-kinase-, cAMP-dependent protein kinase-, and Akt-dependent pathway and leads to endothelial-dependent vasorelaxation. J. Biol. Chem. 2004;279:6190-6195

Ludwig A, Lorenz M, Grimbo N, Steinle F, Meiners S, Bartsch C, Stangl K, Baumann G, Stangl V. The tea flavonoid epigallocatechin-3-gallate reduces cytokine-induced VCAM-1 expression and monocyte adhesion to endothelial cells. Biochem. Biophys. Res. Commun. 2004;316:659-665

To top

Research database

For more details please use the Charité undefinedresearch database.