alexa Apocynin Exerts Dose-Dependent Cardioprotective Effects by Attenuating Reactive Oxygen Species in Ischemia/Reperfusion | OMICS International
ISSN: 2329-6607

Cardiovascular Pharmacology: Open Access
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Research Article

Apocynin Exerts Dose-Dependent Cardioprotective Effects by Attenuating Reactive Oxygen Species in Ischemia/Reperfusion

Qian Chen, Woodworth Parker C, Issachar Devine, Regina Ondrasik, Tsion Habtamu, Kyle D Bartol, Brendan Casey, Harsh Patel, William Chau, Tarah Kuhn, Robert Barsotti and Lindon Young*

Department of Bio-Medical Sciences, Philadelphia College of Osteopathic Medicine, Philadelphia, USA

Corresponding Author:
Lindon Young
Department of Bio-Medical Sciences
Philadelphia College of Osteopathic Medicine (PCOM)
4170 City Avenue, Philadelphia, USA
Tel: 2158716832
Fax: 2158716869
E-mail: [email protected]

Received date: February 16, 2016; Accepted date: February 24, 2016; Published date: March 01, 2016

Citation: Chen Q, Parker WC, Devine I, Ondrasik R, Habtamu T, et al. (2016) Apocynin Exerts Dose-Dependent Cardioprotective Effects by Attenuating Reactive Oxygen Species in Ischemia/Reperfusion. Cardiovasc Pharm Open Access 5:176. doi:10.4172/2329-6607.1000176

Copyright: © 2016 Chen Q, et al. 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

Ischemia/reperfusion results in cardiac contractile dysfunction and cell death partly due to increased reactive oxygen species and decreased endothelial-derived nitric oxide bioavailability. NADPH oxidase normally produces reactive oxygen species to facilitate cell signalling and differentiation; however, excessive release of such species following ischemia exacerbates cell death. Thus, administration of an NADPH oxidase inhibitor, apocynin, may preserve cardiac function and reduce infarct size following ischemia. Apocynin dose-dependently (40 μM, 400 μM and 1 mM) attenuated leukocyte superoxide release by 87 ± 7%. Apocynin was also given to isolated perfused hearts after ischemia, with infarct size decreasing to 39 ± 7% (40 μM), 28 ± 4% (400 μM; p < 0.01) and 29 ± 6% (1 mM; p < 0.01), versus the control’s 46 ± 2%. This decrease correlated with improved final post-reperfusion left ventricular end-diastolic pressure, which decreased from 60 ± 5% in control hearts to 56 ± 5% (40 μM), 43 ± 4% (400 μM; p < 0.01) and 48 ± 5% (1 mM; p < 0.05), compared to baseline. Functionally, apocynin (13.7 mg/kg, I.V.) significantly reduced H2O2 by nearly four-fold and increased endothelial-derived nitric oxide bioavailability by nearly four-fold during reperfusion compared to controls (p < 0.01), which was confirmed in in vivo rat hind limb ischemia/reperfusion models. These results suggest that apocynin attenuates ischemia/reperfusion-induced cardiac contractile dysfunction and infarct size by inhibiting reactive oxygen species release from NADPH oxidase.

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