Probucol Protects Rats from Cardiac Dysfunction Induced by Oxidative Stress following Cardiopulmonary Resuscitation
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 c...
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Series: | Oxidative Medicine and Cellular Longevity |
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doaj-9586af3cf2c14094ae88d2286fe0a9d12020-11-24T23:01:20ZengHindawi LimitedOxidative Medicine and Cellular Longevity1942-09001942-09942017-01-01201710.1155/2017/12848041284804Probucol Protects Rats from Cardiac Dysfunction Induced by Oxidative Stress following Cardiopulmonary ResuscitationXu Xiao0Huiyuan Hou1Victor Lin2Daisy Ho3Kyle Tran4Briana Che5Adam May6Jiancheng Zhang7Zhigang Lu8Zhongping Lu9Peter X. Shaw10Department of Emergency Medicine, Sichuan People’s Hospital, Chengdu 610061, ChinaDepartment of Ophthalmology and Shiley Eye Institute, University of California, San Diego, La Jolla, CA 92093, USADepartment of Ophthalmology and Shiley Eye Institute, University of California, San Diego, La Jolla, CA 92093, USADepartment of Ophthalmology and Shiley Eye Institute, University of California, San Diego, La Jolla, CA 92093, USADepartment of Ophthalmology and Shiley Eye Institute, University of California, San Diego, La Jolla, CA 92093, USADepartment of Ophthalmology and Shiley Eye Institute, University of California, San Diego, La Jolla, CA 92093, USADepartment of Ophthalmology and Shiley Eye Institute, University of California, San Diego, La Jolla, CA 92093, USADepartment of Emergency Medicine, Sichuan People’s Hospital, Chengdu 610061, ChinaDepartment of Ophthalmology and Shiley Eye Institute, University of California, San Diego, La Jolla, CA 92093, USADepartment of Ophthalmology, Huaxi Hospital, Chengdu 610061, ChinaDepartment of Ophthalmology and Shiley Eye Institute, University of California, San Diego, La Jolla, CA 92093, USAObjective. 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.http://dx.doi.org/10.1155/2017/1284804 |
collection |
DOAJ |
language |
English |
format |
Article |
sources |
DOAJ |
author |
Xu Xiao Huiyuan Hou Victor Lin Daisy Ho Kyle Tran Briana Che Adam May Jiancheng Zhang Zhigang Lu Zhongping Lu Peter X. Shaw |
spellingShingle |
Xu Xiao Huiyuan Hou Victor Lin Daisy Ho Kyle Tran Briana Che Adam May Jiancheng Zhang Zhigang Lu Zhongping Lu Peter X. Shaw Probucol Protects Rats from Cardiac Dysfunction Induced by Oxidative Stress following Cardiopulmonary Resuscitation Oxidative Medicine and Cellular Longevity |
author_facet |
Xu Xiao Huiyuan Hou Victor Lin Daisy Ho Kyle Tran Briana Che Adam May Jiancheng Zhang Zhigang Lu Zhongping Lu Peter X. Shaw |
author_sort |
Xu Xiao |
title |
Probucol Protects Rats from Cardiac Dysfunction Induced by Oxidative Stress following Cardiopulmonary Resuscitation |
title_short |
Probucol Protects Rats from Cardiac Dysfunction Induced by Oxidative Stress following Cardiopulmonary Resuscitation |
title_full |
Probucol Protects Rats from Cardiac Dysfunction Induced by Oxidative Stress following Cardiopulmonary Resuscitation |
title_fullStr |
Probucol Protects Rats from Cardiac Dysfunction Induced by Oxidative Stress following Cardiopulmonary Resuscitation |
title_full_unstemmed |
Probucol Protects Rats from Cardiac Dysfunction Induced by Oxidative Stress following Cardiopulmonary Resuscitation |
title_sort |
probucol protects rats from cardiac dysfunction induced by oxidative stress following cardiopulmonary resuscitation |
publisher |
Hindawi Limited |
series |
Oxidative Medicine and Cellular Longevity |
issn |
1942-0900 1942-0994 |
publishDate |
2017-01-01 |
description |
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. |
url |
http://dx.doi.org/10.1155/2017/1284804 |
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