Literature DB >> 21651898

Zinc pyrithione salvages reperfusion injury by inhibiting NADPH oxidase activation in cardiomyocytes.

Viswanath Kasi1, Sreedhar Bodiga, Upendra Nadh Kommuguri, Suneetha Sankuru, Vijaya Lakshmi Bodiga.   

Abstract

Zinc pyrithione (ZPT), has a strong anti-apoptotic effect when administered just before reperfusion. Because oxidative stress has been proposed to contribute to myocardial reperfusion injury, we tested whether ZPT can reduce the production of reactive oxygen species during reoxygenation in cultured neonatal rat cardiac myocytes and evaluated the role of NADPH oxidase in hypoxia/reoxygenation (H/R) injury. The cells were subjected to 8h of simulated ischemia, followed by either 30 min or 16 h of reoxygenation. ZPT when started just before reoxygenation significantly reduced superoxide generation, LDH release and improved cell survival compared to H/R. Attenuation of the ROS production by ZPT paralleled its capacity to prevent pyknotic nuclei formation. In addition, ZPT reversed the H/R-induced expression of NOX2 and p47(phox) phosphorylation indicating that ZPT directly protects cardiomyocytes from reperfusion injury by a mechanism that attenuates NADPH oxidase mediated intracellular oxidative stress.
Copyright © 2011 Elsevier Inc. All rights reserved.

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Year:  2011        PMID: 21651898     DOI: 10.1016/j.bbrc.2011.05.130

Source DB:  PubMed          Journal:  Biochem Biophys Res Commun        ISSN: 0006-291X            Impact factor:   3.575


  6 in total

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Review 4.  Current status of NADPH oxidase research in cardiovascular pharmacology.

Authors:  Bruno K Rodiño-Janeiro; Beatriz Paradela-Dobarro; María Isabel Castiñeiras-Landeira; Sergio Raposeiras-Roubín; José R González-Juanatey; Ezequiel Alvarez
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Review 6.  The Oxidative Balance Orchestrates the Main Keystones of the Functional Activity of Cardiomyocytes.

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  6 in total

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