Complex effects of different green tea catechins on human platelets

被引:52
作者
Lill, G [1 ]
Voit, S [1 ]
Schrör, K [1 ]
Weber, AA [1 ]
机构
[1] Univ Klinikum Dusseldorf, Inst Pharmakol & Klin Pharmakol, D-40225 Dusseldorf, Germany
关键词
green tea; catechin; epigallocatechin gallate; platelet; aggregation;
D O I
10.1016/S0014-5793(03)00599-4
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Epigallocatechin gallate (EGCG), a major component of green tea, has been previously shown to inhibit platelet aggregation. The effects of other green tea catechins on platelet function are not known. Pre-incubation with EGCG concentration-dependently inhibited thrombin-induced aggregation and phosphorylation of p38 mitogen-activated protein kinase and extracellular signal-regulated kinases-1/2. In contrast EGCG stimulated tyrosine phosphorylation of platelet proteins, including Syk and SLP-76 but inhibited phosphorylation of focal adhesion kinase. Other catechins did not inhibit platelet aggregation. Interestingly, when EGCG was added to stirred platelets, a tyrosine kinase-dependent stimulation of platelet aggregation was observed. The other two catechins containing a galloyl group in the 3' position (catechin gallate, epicatechin gallate) also stimulated platelet aggregation, while catechins without a galloyl group (catechin, epicatechin) or the catechin with a galloyl group in the 2' position (epigallocatechin) did not. (C) 2003 Published by Elsevier Science B.V. on behalf of the Federation of European Biochemical Societies.
引用
收藏
页码:265 / 270
页数:6
相关论文
共 28 条
[1]   Epigallocathechin-3 gallate selectively inhibits the PDGF-BB-induced intracellular signaling transduction pathway in vascular smooth muscle cells and inhibits transformation of sis-transfected NIH 3T3 fibroblasts and human glioblastoma cells (A172) [J].
Ahn, HY ;
Hadizadeh, KR ;
Seul, C ;
Yun, YP ;
Vetter, H ;
Sachinidis, A .
MOLECULAR BIOLOGY OF THE CELL, 1999, 10 (04) :1093-1104
[2]   (+)-catechin inhibits platelet hyperactivity induced by an acute iron load in vivo [J].
Blache, D ;
Durand, P ;
Prost, M ;
Loreau, N .
FREE RADICAL BIOLOGY AND MEDICINE, 2002, 33 (12) :1670-1680
[3]   FLAVONOIDS INHIBIT THE OXIDATIVE MODIFICATION OF LOW-DENSITY LIPOPROTEINS BY MACROPHAGES [J].
DEWHALLEY, CV ;
RANKIN, SM ;
HOULT, JRS ;
JESSUP, W ;
LEAKE, DS .
BIOCHEMICAL PHARMACOLOGY, 1990, 39 (11) :1743-1750
[4]   Antihypertensive effects of the flavonoid quercetin in spontaneously hypertensive rats [J].
Duarte, J ;
Pérez-Palencia, R ;
Vargas, F ;
Ocete, MA ;
Pérez-Vizcaino, F ;
Zarzuelo, A ;
Tamargo, J .
BRITISH JOURNAL OF PHARMACOLOGY, 2001, 133 (01) :117-124
[5]   Tea flavonoids may protect against atherosclerosis -: The Rotterdam study [J].
Geleijnse, JM ;
Launer, LJ ;
Hofman, A ;
Pols, HAP ;
Witteman, JCM .
ARCHIVES OF INTERNAL MEDICINE, 1999, 159 (18) :2170-2174
[6]   Transduction - Integrin signaling [J].
Giancotti, FG ;
Ruoslahti, E .
SCIENCE, 1999, 285 (5430) :1028-1032
[7]   GREEN TEA COMPOSITION, CONSUMPTION, AND POLYPHENOL CHEMISTRY [J].
GRAHAM, HN .
PREVENTIVE MEDICINE, 1992, 21 (03) :334-350
[8]   Advances in flavonoid research since 1992 [J].
Harborne, JB ;
Williams, CA .
PHYTOCHEMISTRY, 2000, 55 (06) :481-504
[9]   Platelet CD40 ligand (CD40L) -: subcellular localization, regulation of expression, and inhibition by clopidogrel [J].
Hermann, A ;
Rauch, BH ;
Braun, M ;
Schrör, K ;
Weber, AA .
PLATELETS, 2001, 12 (02) :74-82
[10]   DIETARY ANTIOXIDANT FLAVONOIDS AND RISK OF CORONARY HEART-DISEASE - THE ZUTPHEN ELDERLY STUDY [J].
HERTOG, MGL ;
FESKENS, EJM ;
HOLLMAN, PCH ;
KATAN, MB ;
KROMHOUT, D .
LANCET, 1993, 342 (8878) :1007-1011