Anti-platelet effects of epigallocatechin-3-gallate in addition to the concomitant aspirin, clopidogrel or ticagrelor treatment
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Background/Aims: Although epigallocatechin-3-gallate (EGCG), which is found in high contents in the dried leaves of green tea, has been reported to have an anti- platelet effect, synergistic effects of EGCG in addition to current anti-platelet medications remains to be elucidated. Methods: Blood samples were obtained from 40 participants who took aspirin (ASA, n = 10), clopidogrel (CPD, n = 10), ticagrelor (TCG, n = 10) and no anti-platelet medication (Control, n = 10). Ex vivo platelet aggregation and adhesion under various stimulators were analyzed by multiple electrode aggregometry (MEA) and Impact-R systems. PAC-1 and P-selectin expressions in human platelets were analyzed by flow cytometry. Results: In MEA analysis, adenosine diphosphate (ADP) and thrombin receptor activating peptide (TRAP)-induced platelet aggregations were lower in the CPD and the TCG groups; arachidonic acid (AA)-induced platelet aggregation was lower in the ASA group, whereas collagen (COL)-induced platelet aggregations were comparable among four groups. EGCG significantly reduced ADP- and COL-induced platelet aggregation in dose-dependent manner (ADP, p = 0.04; COL, p < 0.01). There were no additional suppressions of platelet aggregation stimulated by AA in the ASA group, and by ADP in the CPD and TCG groups. Moreover, EGCG suppressed shear stress-induced platelet adhesion on Impact-R, and had no effect on P-selectin and PAC-1 expressions. Conclusions: Ex vivo treatment of EGCG inhibited platelet adhesion and aggregation without changes in P-selectin and PAC-1 expression. There was no additional suppressions in platelet aggregation stimulated by AA in the ASA group and ADP in the CPD and TCG groups.
Abstract
Background/Aims: Although epigallocatechin-3-gallate (EGCG), which is found in high contents in the dried leaves of green tea, has been reported to have an anti- platelet effect, synergistic effects of EGCG in addition to current anti-platelet medications remains to be elucidated. Methods: Blood samples were obtained from 40 participants who took aspirin (ASA, n = 10), clopidogrel (CPD, n = 10), ticagrelor (TCG, n = 10) and no anti-platelet medication (Control, n = 10). Ex vivo platelet aggregation and adhesion under various stimulators were analyzed by multiple electrode aggregometry (MEA) and Impact-R systems. PAC-1 and P-selectin expressions in human platelets were analyzed by flow cytometry. Results: In MEA analysis, adenosine diphosphate (ADP) and thrombin receptor activating peptide (TRAP)-induced platelet aggregations were lower in the CPD and the TCG groups; arachidonic acid (AA)-induced platelet aggregation was lower in the ASA group, whereas collagen (COL)-induced platelet aggregations were comparable among four groups. EGCG significantly reduced ADP- and COL-induced platelet aggregation in dose-dependent manner (ADP, p = 0.04; COL, p < 0.01). There were no additional suppressions of platelet aggregation stimulated by AA in the ASA group, and by ADP in the CPD and TCG groups. Moreover, EGCG suppressed shear stress-induced platelet adhesion on Impact-R, and had no effect on P-selectin and PAC-1 expressions. Conclusions: Ex vivo treatment of EGCG inhibited platelet adhesion and aggregation without changes in P-selectin and PAC-1 expression. There was no additional suppressions in platelet aggregation stimulated by AA in the ASA group and ADP in the CPD and TCG groups.
참고문헌 (36)
- D'Ascenzo F, "Meta-analysis of randomized controlled trials and adjusted observational results of use of clopidogrel, aspirin, and oral anticoagulants in patients undergoing percutaneous coronary intervention", Am J Cardiol, 115, pp.1185~1193 (2015)[DOI]
- 진한영, "Randomized Comparison of the Platelet Inhibitory Efficacy between Low Dose Prasugrel and Standard Dose Clopidogrel in Patients Who Underwent Percutaneous Coronary Intervention", Korean Circulation Journal, 44(2), pp.82~88 (2014), 대한심장학회
- Levine GN, "2011 ACCF", AHA, American Heart Association Task Force on Practice Guidelines and the Society for Cardiovascular Angiography and Interventions, pp.Circulation, 2011[DOI]
- Li J, "Laboratory aspirin resistance and the risk of major adverse cardiovascular events in patients with coronary heart disease on confirmed aspirin adherence", J Atheroscler Thromb, 21, pp.239~247 (2014)[DOI]
- Muller I, "Prevalence of clopidogrel non-responders among patients with stable angina pectoris scheduled for elective coronary stent placement", Thromb Haemost, 89, pp.783~787 (2003)[DOI]
- Lev EI, "Aspirin and clopidogrel drug response in patients undergoing percutaneous coronary intervention: the role of dual drug resistance", J Am Coll Cardiol, 47, pp.27~33 (2006)[DOI]
- Campo G, "Long-term clinical outcome based on aspirin and clopidogrel responsiveness status after elective percutaneous coronary intervention: a 3T", 2R (tailoring treatment with tirofiban in patients showing resistance to aspirin and, J Am Coll Cardiol, pp.2010, 56[DOI]
- Cuisset T, "Post-PCI fatal bleeding in aspirin and clopidogrel hyper responder: shifting from antiplatelet resistance to bleeding risk assessment?", Int J Cardiol, 138, pp.212~213 (2010)[DOI]
- Shimizu M, "Targeting receptor tyrosine kinases for chemoprevention by green tea catechin, EGCG", Int J Mol Sci, 9, pp.1034~1049 (2008)[DOI]
- Lee HS, "Epigalloccatechin- 3-gallate inhibits ocular neovascularization and vascular permeability in human retinal pigment epithelial and human retinal microvascular endothelial cells via suppression of MMP-9 and VEGF activation", Molecules, 19, pp.12150~12172 (2014)[DOI]
- Sugisawa A, "Physiological concentrations of (-)-epigallocatechin-3-O-gallate (EGCg) prevent chromosomal damage induced by reactive oxygen species in WIL2-NS cells", J Nutr, 132, pp.1836~1839 (2002)[DOI]
- Deana R, "Green tea epigallocatechin- 3-gallate inhibits platelet signaling pathways triggered by both proteolytic and non-proteolytic agonists", Thromb Haemost, 89, pp.866~874 (2003)[DOI]
- Matsumura K, "Preservation of platelets by adding epigallocatechin-3-o-gallate to platelet concentrates", Cell Transplant, 18, pp.521~528 (2009)[DOI]
- Sibbing D, "Assessment of ADP-induced platelet aggregation with light transmission aggregometry and multiple electrode platelet aggregometry before and after clopidogrel treatment", Thromb Haemost, 99, pp.121~126 (2008)
- Shenkman B, "Variable responsiveness to clopidogrel and aspirin among patients with acute coronary syndrome as assessed by platelet function tests", Thromb Res, 122, pp.336~345 (2008)[DOI]
- Scheer FA, "The human endogenous circadian system causes greatest platelet activation during the biological morning independent of behaviors", PLoS One, 6, pp.e24549~ (2011)[DOI]
- Chowdhury A, "Protective role of epigallocatechin-3-gallate in health and disease: a perspective", Biomed Pharmacother, 78, pp.50~59 (2016)[DOI]
- Sagesaka-Mitane Y, "Platelet aggregation inhibitors in hot water extract of green tea", Chem Pharm Bull (Tokyo), 38, pp.790~793 (1990)[DOI]
- Kang WS, "Antithrombotic activities of green tea catechins and (-)-epigallocatechin gallate", Thromb Res, 96, pp.229~237 (1999)[DOI]
- 주승재, "An Assay of Measuring Platelet Reactivity Using Monoclonal Antibody against Activated Platelet Glycoprotein IIb", IIIa in Patients Taking Clopidogrel, 2015, pp.45(5), 378~385[DOI]
- Li Z, "Signaling during platelet adhesion and activation", Arterioscler Thromb Vasc Biol, 30, pp.2341~2349 (2010)[DOI]
- Kang WS, "Antiplatelet activity of green tea catechins is mediated by inhibition of cytoplasmic calcium increase", J Cardiovasc Pharmacol, 38, pp.875~884 (2001)[DOI]
- Ok WJ, "Epigallocatechin-3-gallate has an anti-platelet effect in a cyclic AMP-dependent manner", J Atheroscler Thromb, 19, pp.337~348 (2012)[DOI]
- Lill G, "Complex effects of different green tea catechins on human platelets", FEBS Lett, 546, pp.265~270 (2003)[DOI]
- Neuhaus T, "Platelet aggregation induced by the C-terminal peptide of thrombospondin-1 (4N1-1) is inhibited by epigallocatechin gallate but not by prostaglandin E1", Platelets, 15, pp.455~457 (2004)[DOI]
- 이동하, "Inhibitory Effects of Epigallocatechin-3-Gallate on Microsomal Cyclooxygenase-1 Activity in Platelets", Biomolecules & Therapeutics, 21(1), pp.54~59 (2013), 한국응용약물학회
- Iida Y, "(-)-Epigallocatechin gallate selectively inhibits adenosine diphosphatestimulated human platelet activation: suppression of heat shock protein 27 phosphorylation via p38 mitogenactivated protein kinase", Mol Med Rep, 10, pp.1383~1388 (2014)[DOI]
- Wijeyeratne YD, "Anti-platelet therapy: ADP receptor antagonists", Br J Clin Pharmacol, 72, pp.647~657 (2011)[DOI]
- Wong AK, "Platelet biology: the role of shear", Expert Rev Hematol, 6, pp.205~212 (2013)[DOI]
- Frelinger AL 3rd, "Platelet function tests, independent of platelet count, are associated with bleeding severity in ITP", Blood, 126, pp.873~879 (2015)[DOI]
- Floyd CN, "Antiplatelet drug resistance: molecular insights and clinical implications", Prostaglandins Other Lipid Mediat, 120, pp.21~27 (2015)[DOI]
- Sorensen R, "Risk of bleeding related to antithrombotic treatment in cardiovascular disease", Curr Pharm Des, 18, pp.5362~5378 (2012)[DOI]
- Keske MA, "Vascular and metabolic actions of the green tea polyphenol epigallocatechin gallate", Curr Med Chem, 22, pp.59~69 (2015)
- Legeay S, "Epigallocatechin gallate: a review of its beneficial properties to prevent metabolic syndrome", Nutrients, 7, pp.5443~5468 (2015)[DOI]
- Manach C, "Bioavailability and bioefficacy of polyphenols in humans. I. Review of 97 bioavailability studies", Am J Clin Nutr, 81, pp.230S~242S (2005)[DOI]
- Williamson G, "Flavanols from green tea and phenolic acids from coffee: critical quantitative evaluation of the pharmacokinetic data in humans after consumption of single doses of beverages", Mol Nutr Food Res, 55, pp.864~873 (2011)[DOI]