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Evidence-Based Complementary and Alternative Medicine
Volume 2013 (2013), Article ID 595128, 9 pages
http://dx.doi.org/10.1155/2013/595128
Research Article

Novel Bioactivity of Ellagic Acid in Inhibiting Human Platelet Activation

1Department of Anesthesiology, Shin Kong Wu Ho-Su Memorial Hospital, Taipei 111, Taiwan
2School of Medicine, Fu Jen Catholic University, Taipei 242, Taiwan
3Graduate Institute of Medical Sciences, Taipei Medical University, 250 Wu-Hsing Street, Taipei 110, Taiwan
4Department of Pharmacology, Taipei Medical University, 250 Wu-Hsing Street, Taipei 110, Taiwan
5Department of Cardiology, Cathay General Hospital, Section 4, No. 280, Jen-Ai Road, Taipei 106, Taiwan

Received 6 December 2012; Accepted 4 January 2013

Academic Editor: Tzeng-Ji Chen

Copyright © 2013 Yi 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.

Abstract

Pomegranates are widely consumed either as fresh fruit or in beverage form as juice and wine. Ellagic acid possesses potent antioxidative properties; it is known to be an effective phytotherapeutic agent with antimutagenic and anticarcinogenic qualities. Ellagic acid (20 to 80 μM) exhibited a potent activity in inhibiting platelet aggregation stimulated by collagen; however, it did not inhibit platelet aggregation stimulated by thrombin, arachidonic acid, or U46619. Treatment with ellagic acid (50 and 80 μM) significantly inhibited platelet activation stimulated by collagen; this alteration was accompanied by the inhibition of relative mobilization, and the phosphorylation of phospholipase C (PLC)γ2, protein kinase C (PKC), mitogen-activated protein kinases (MAPKs), and Akt, as well as hydroxyl radical (OH) formation. In addition, ellagic acid also inhibited p38 MAPK and Akt phosphorylation stimulated by hydrogen peroxide. By contrast, ellagic acid did not significantly affect PKC activation and platelet aggregation stimulated by PDBu. This study is the first to show that, in addition to being considered a possible agent for preventing tumor growth, ellagic acid possesses potent antiplatelet properties. It appears to initially inhibit the PLC 2-PKC cascade and/or hydroxyl radical formation, followed by decreased phosphorylation of MAPKs and Akt, ultimately inhibiting platelet aggregation.