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Oxidative Medicine and Cellular Longevity
Volume 2016, Article ID 5868913, 11 pages
http://dx.doi.org/10.1155/2016/5868913
Research Article

Exercise Training Attenuates Upregulation of p47phox and p67phox in Hearts of Diabetic Rats

1Department of Cellular & Integrative Physiology, University of Nebraska Medical Center, Omaha, NE 68198, USA
2Division of Cardiology, University of Nebraska Medical Center, Omaha, NE 68198, USA

Received 14 July 2015; Revised 24 September 2015; Accepted 21 December 2015

Academic Editor: José Luís García-Giménez

Copyright © 2016 Neeru M. Sharma 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

Exercise training (ExT) is currently being used as a nonpharmacological strategy to improve cardiac function in diabetic patients. However, the molecular mechanism(s) underlying its beneficial effects remains poorly understood. Oxidative stress is known to play a key role in the pathogenesis of diabetic cardiomyopathy and one of the enzyme systems that produce reactive oxygen species is NADH/NADPH oxidase. The goal of this study was to investigate the effect of streptozotocin- (STZ-) induced diabetes on expression of and , key regulatory subunits of NADPH oxidase, in cardiac tissues and determine whether ExT can attenuate these changes. Four weeks after STZ treatment, expression of and increased 2.3-fold and 1.6-fold, respectively, in left ventricles of diabetic rats and these increases were attenuated with three weeks of ExT, initiated 1 week after onset of diabetes. In atrial tissues, there was increased expression of (74%), which was decreased by ExT in diabetic rats. Furthermore, increased collagen III levels in diabetic hearts (52%) were significantly reduced by ExT. Taken together, ExT attenuates the increased expression of and in the hearts of diabetic rats which could be an underlying mechanism for improving intracardiac matrix and thus cardiac function and prevent cardiac remodeling in diabetic cardiomyopathy.