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Oxidative Medicine and Cellular Longevity
Volume 2016 (2016), Article ID 3196431, 9 pages
http://dx.doi.org/10.1155/2016/3196431
Research Article

Spironolactone Effect in Hepatic Ischemia/Reperfusion Injury in Wistar Rats

1Liver Unit, Department of Internal Medicine, University Hospital “Dr. José E. González”, The Autonomous University of Nuevo León, 64460 Monterrey, NL, Mexico
2Hospital Regional de Alta Especialidad de Ciudad Victoria “Bicentenario 2010”, 87087 Cuidad Victoria, TAMPS, Mexico
3Transplant Service, University Hospital “Dr. José E. González”, The Autonomous University of Nuevo León, 64460 Monterrey, NL, Mexico
4Department of Pathology, University Hospital “Dr. José E. González”, The Autonomous University of Nuevo León, 64460 Monterrey, NL, Mexico
5Department of Physiology, School of Medicine, The Autonomous University of Nuevo León, 64460 Monterrey, NL, Mexico

Received 24 July 2015; Revised 7 October 2015; Accepted 11 October 2015

Academic Editor: Karina R. Gordillo

Copyright © 2016 Julio César Jiménez Pérez et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Abstract

Introduction. Ischemia/reperfusion (IR) injury, often associated with liver surgery, is an unresolved problem in the clinical practice. Spironolactone is an antagonist of aldosterone that has shown benefits over IR injury in several tissues, but its effects in hepatic IR are unknown. Objective. To evaluate the effect of spironolactone on IR-induced damage in liver. Materials and Methods. Total hepatic ischemia was induced in rats for 20 min followed by 60 min of reperfusion. Spironolactone was administered and hepatic injury, cytokine production, and oxidative stress were assessed. Results. After IR, increased transaminases levels and widespread acute inflammatory infiltrate, disorganization of hepatic hemorrhage trabeculae, and presence of apoptotic bodies were observed. Administration of SPI reduced biochemical and histological parameters of liver injury. SPI treatment increased IL-6 levels when compared with IR group but did not modify either IL-1β or TNF-α with respect to IR group. Regarding oxidative stress, increased levels of catalase activity were recorded in IR + SPI group in comparison with group without treatment, whereas MDA levels were similar in IR + SPI and IR groups. Conclusions. Spironolactone reduced the liver damage induced by IR, and this was associated with an increase in IL-6 production and catalase activity.