Antiplatelet and calcium inhibitory properties of eugenol and sodium eugenol acetate |
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| Institution: | 1. Department of Internal Medicine and The Molecular Medicine Program, University of Utah, Salt Lake City, UT, USA;2. Department of Pathology, University of Utah, Salt Lake City, UT, USA;3. Department of Cardiology and Cardiovascular Medicine, University of Tübingen, Tübingen, Germany;4. Department of Internal Medicine, GRECC, George E. Wahlen VAMC, Salt Lake City, UT, USA;1. Kusuma School of Biological Sciences, Indian Institute of Technology, Delhi, New Delhi 110016, India.;2. Integrative Parasitology, Department of Infectious Diseases, University of Heidelberg Medical School, Im Neuenheimer Feld 324, 69120 Heidelberg, Germany.;1. Centre for Molecular and Biomolecular Informatics, Radboud University Medical Center, Geert Grooteplein-Zuid 26-28, 6525 GA Nijmegen, The Netherlands;2. Department of Biochemistry, Netherlands Cancer Institute, Plesmanlaan 121, 1066 CX Amsterdam, The Netherlands |
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| Abstract: | - 1.1. Eugenol (3-methoxy-4-hydroxy-propenylbenzene) or sodium eugenol acetate (4-0-acetic acid sodium-3-methoxy-l-propenylbenzene) (0.25, 0.5, 1 mM) concentration-dependently inhibited arachidonic acid (AA)., collagen-, epinephrine- and ADP-induced platelet aggregation.
- 2.2. Eugenol or sodium eugenol acetate inhibited collagen-induced aggregation of washed rabbit platelets synergistically with creatine phosphatelcreatine phosphokinase (CP/CPK, 5 mM/10 U/ml) or p-bromophenacyl bromide (p-BPB, 10 μM), and they also potentiated the inhibitory action of imidazole (0.5 mM) on AA-induced aggregation.
- 3.3. Eugenol or sodium eugenol acetate (0.25, 0.5, 1 mM) concentration-dependently inhibited AA-induced thromboxane B2 and prostaglandin E2 formation.
- 4.4. The rise of intracellular Ca2+ caused by collagen, epinephrine, ADP, and AA were inhibited by eugenol or sodium eugenol acetate (1 mM).
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