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Evidence-Based Complementary and Alternative Medicine
Volume 2012 (2012), Article ID 683872, 8 pages
Research Article

Gallic Acid Attenuates Platelet Activation and Platelet-Leukocyte Aggregation: Involving Pathways of Akt and GSK3β

1Graduate Institute of Clinical Medical Science, China Medical University, Taichung 40402, Taiwan
2Division of Cardiology, Department of Medicine, China Medical University Hospital, Taichung 40407, Taiwan
3Department of Psychiatry, China Medical University Hospital, Taichung 40407, Taiwan
4Department of Anesthesiology, China Medical University Hospital, Taichung 40407, Taiwan
5Graduate Institute of Anatomy and Cell Biology, College of Medicine, National Taiwan University, Taipei 10051, Taiwan

Received 19 February 2012; Revised 8 May 2012; Accepted 15 May 2012

Academic Editor: I-Min Liu

Copyright © 2012 Shih-Sheng Chang et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


Platelet activation and its interaction with leukocytes play an important role in atherothrombosis. Cardiovascular diseases resulted from atherothrombosis remain the major causes of death worldwide. Gallic acid, a major constituent of red wine and tea, has been believed to have properties of cardiovascular protection, which is likely to be related to its antioxidant effects. Nonetheless, there were few and inconsistent data regarding the effects of gallic acid on platelet function. Therefore, we designed this in vitro study to determine whether gallic acid could inhibit platelet activation and the possible mechanisms. From our results, gallic acid could concentration-dependently inhibit platelet aggregation, P-selectin expression, and platelet-leukocyte aggregation. Gallic acid prevented the elevation of intracellular calcium and attenuated phosphorylation of PKCα/p38 MAPK and Akt/GSK3β on platelets stimulated by the stimulants ADP or U46619. This is the first mechanistic explanation for the inhibitory effects on platelets from gallic acid.