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Oxidative Medicine and Cellular Longevity
Volume 2017, Article ID 1284804, 10 pages
Research Article

Probucol Protects Rats from Cardiac Dysfunction Induced by Oxidative Stress following Cardiopulmonary Resuscitation

1Department of Emergency Medicine, Sichuan People’s Hospital, Chengdu 610061, China
2Department of Ophthalmology and Shiley Eye Institute, University of California, San Diego, La Jolla, CA 92093, USA
3Department of Neurology, First People’s Hospital of Jingmen, Jingmen, Hubei Province 448000, China
4Department of Ophthalmology, Huaxi Hospital, Chengdu 610061, China

Correspondence should be addressed to Xu Xiao; moc.361@3211iyoaixgnay and Peter X. Shaw; ude.dscu@wahsp

Received 28 March 2017; Revised 2 June 2017; Accepted 21 June 2017; Published 30 October 2017

Academic Editor: Fiona L. Wilkinson

Copyright © 2017 Xu Xiao 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.


Objective. To investigate the protective effect of probucol on induced cardiac arrest (CA) rats and possible mechanisms. Methods. Sprague Dawley rats were orally administrated with probucol at different dosage or vehicle for 5 days and subjected to a CA model by electrical stimulation, followed by cardiopulmonary resuscitation (CPR). The return of spontaneous circulation (ROSC) rate, antioxidant enzyme activities, and lipid oxidation markers were measured in serum and myocardium. Hemodynamic parameters and myocardial functions of animals were analyzed. Expression of erythroid-derived 2-like 2 (NFE2L2) and Kelch-like ECH-associated protein 1 (KEAP1) in the myocardium were examined with immunohistochemistry. Results. Probucol treatment significantly increased the ROSC rate and survival time of CA-induced rats. After ROSC, levels of oxidation-specific markers were decreased, while activities of antioxidant enzymes were increased significantly in probucol treatment groups. The probucol treatment improves hemodynamic parameters and myocardial functions. These parameter changes were in a dose-dependent manner. In the probucol treatment groups, the expression of KEAP1 was downregulated, while that of NFE2L2 was upregulated significantly. Conclusion. In the CA-induced rat model, probucol dose dependently improved the ROSC rate, prolonged survival time, alleviated oxidative stress, and improved cardiac function. Such protective effects are possibly through regulations of the KEAP1-NFE2L2 system.