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Anti-platelet effects of epigallocatechin-3-gallate in addition to the concomitant aspirin, clopidogrel or ticagrelor treatment

  • Joo, Hyung Joon (Department of Cardiology, Cardiovascular Center, Korea University Anam Hospital) ;
  • Park, Ji-Young (Department of Clinical Pharmacology and Toxicology, Korea University Anam Hospital) ;
  • Hong, Soon Jun (Department of Cardiology, Cardiovascular Center, Korea University Anam Hospital) ;
  • Kim, Kyoung-Ah (Department of Clinical Pharmacology and Toxicology, Korea University Anam Hospital) ;
  • Lee, Seung Hoon (Department of Cardiology, Cardiovascular Center, Korea University Anam Hospital) ;
  • Cho, Jae-Young (Department of Cardiology, Cardiovascular Center, Korea University Anam Hospital) ;
  • Park, Jae Hyoung (Department of Cardiology, Cardiovascular Center, Korea University Anam Hospital) ;
  • Yu, Cheol Woong (Department of Cardiology, Cardiovascular Center, Korea University Anam Hospital) ;
  • Lim, Do-Sun (Department of Cardiology, Cardiovascular Center, Korea University Anam Hospital)
  • 투고 : 2016.07.14
  • 심사 : 2017.01.04
  • 발행 : 2018.05.01

초록

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.

키워드

과제정보

연구 과제 주관 기관 : Korea Health Industry Development Institute (KHIDI), National Research Foundation of Korea (NRF)

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