alexa Paraoxonase-1 Deficiency does not Influence Clopidogrel Antiplatelet Function in Mice | OMICS International | Abstract
ISSN: 2329-6607

Cardiovascular Pharmacology: Open Access
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Short Communication

Paraoxonase-1 Deficiency does not Influence Clopidogrel Antiplatelet Function in Mice

Anabel García-Heredia, Anna Hérnandez-Aguilera, Isabel Fort-Gallifa, Jorge Joven, Vicente Martín-Paredero and Jordi Camps*

Unitat de Recerca Biomèdica (AGH, AHA, IFG, JJ, JC), Hospital Universitari de Sant Joan and the Service of Angiology, Vascular Surgery and Endosurgery, Hospital Universitari Joan XXIII (VMP), Institut d’Investigació Sanitària Pere Virgili (IISPV), Universitat Rovira i Virgili, Spain

*Corresponding Author:
Jordi Camps
Unitat de Recerca Biomèdica
Hospital Universitari de Sant Joan
C/ Sant Joan s/n, 43201 Reus, Spain
Tel: +34 977 310 300
E-mail: [email protected]

Received date: June 15, 2015; Accepted date: July 06, 2015; Published date: July 12, 2015

Citation: García-Heredia A, Hérnandez-Aguilera A, Fort-Gallifa I, Joven J,Camps J, et al. (2015) Paraoxonase-1 Deficiency does not Influence Clopidogrel Antiplatelet Function in Mice. Cardiol Pharmacol 4:148. doi: 10.4172/2329-6607.1000148

Copyright: © 2015 García-Heredia A. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

Abstract

Abstract Background: Clopidogrel is an antiplatelet agent used in the treatment of vascular diseases. It requires in vivo bio activation linked to the cytochrome P450. Several studies reported that paraoxonase-1 (PON1) was a crucial enzyme in clopidogrel activation, and that patients carrying a variant of the PON1192 gene polymorphism have a high risk of thrombosis. However, these reports were not confirmed by subsequent results. The present study was aimed at investigating whether PON1 deficiency affects the biological action of clopidogrel in mice. Methods: PON1-deficient mice (n = 50) and wild type animals (n = 50) received different treatments for 3 days: a) clopidogrel, b) aspirin, c) cilostazol, d) clopidogrel + aspirin, and e) clopidogrel + aspirin + cilostazol. Blood was collected for the Platelet Function Analysis (PFA-100). Results: The different anticoagulant treatments resulted in higher aggregation times in all the mice, compared to the internal PFA control; demonstrating the anti-platelet effect of these compounds. We did not observe any significant alterations on the PFA assay in PON1-deficient mice, relative to wild type animals. Conclusion: PON1 deficiency does not influence the antiplatelet action of clopidogrel in mice, and supports the proposition that this enzyme is not involved in clopidogrel bio activation.

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