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

Hyung Joon Joo, Ji-Young Park, Soon Jun Hong, Kyoung Ah Kim, Seung Hoon Lee, Jae Young Cho, Jae Hyoung Park, Cheol Woong Yu, Do-Sun Lim

Research output: Contribution to journalArticle

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-in-duced 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.

Original languageEnglish
Pages (from-to)522-531
Number of pages10
JournalKorean Journal of Internal Medicine
Volume33
Issue number3
DOIs
Publication statusPublished - 2018 May 1

Fingerprint

clopidogrel
Platelet Aggregation
Aspirin
Blood Platelets
Adenosine Diphosphate
P-Selectin
Arachidonic Acid
thrombin receptor peptide SFLLRNP
Collagen
Electrodes
Ticagrelor
epigallocatechin gallate
Tea

Keywords

  • Aspirin
  • Catechin
  • Clopidogrel
  • Platelet inhibitors
  • Ticagrelor

ASJC Scopus subject areas

  • Internal Medicine

Cite this

Anti-platelet effects of epigallocatechin-3-gallate in addition to the concomitant aspirin, clopidogrel or ticagrelor treatment. / Joo, Hyung Joon; Park, Ji-Young; Hong, Soon Jun; Kim, Kyoung Ah; Lee, Seung Hoon; Cho, Jae Young; Park, Jae Hyoung; Yu, Cheol Woong; Lim, Do-Sun.

In: Korean Journal of Internal Medicine, Vol. 33, No. 3, 01.05.2018, p. 522-531.

Research output: Contribution to journalArticle

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AU - Joo, Hyung Joon

AU - Park, Ji-Young

AU - Hong, Soon Jun

AU - Kim, Kyoung Ah

AU - Lee, Seung Hoon

AU - Cho, Jae Young

AU - Park, Jae Hyoung

AU - Yu, Cheol Woong

AU - Lim, Do-Sun

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AB - 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-in-duced 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.

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