Zinc pyrithione salvages reperfusion injury by inhibiting NADPH oxidase activation in cardiomyocytes |
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| Authors: | Kasi Viswanath Bodiga Sreedhar Kommuguri Upendra Nadh Sankuru Suneetha Bodiga Vijaya Lakshmi |
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| Institution: | aDepartment of Pharmacology, Andhra University, Visakhapatnam, Andhra Pradesh, India;bDepartment of Medicine, University of Alberta, Edmonton, Canada T6G 2G3;cDepartment of Biotechnology, Krishna University, Machilipatnam, Andhra Pradesh 521 001, India |
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| 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 8 h 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 p47phox phosphorylation indicating that ZPT directly protects cardiomyocytes from reperfusion injury by a mechanism that attenuates NADPH oxidase mediated intracellular oxidative stress. |
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| Keywords: | Abbreviations: H/R hypoxia/reoxygenation NRCM neonatal rat cardiac myocytes ZPT zinc pyrithione LDH lactate dehydrogenase NOX NADPH oxidase DHE dihydroethidium ROS reactive oxygen species |
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