Hydroxytyrosol Protects against Myocardial Ischemia/Reperfusion Injury through a PI3K/Akt-Dependent Mechanism

Objective. To investigate the effects and mechanisms of hydroxytyrosol (HT) during the pathogenesis of myocardial ischemia reperfusion (I/R) in rat hearts. Methods. The rats were randomized into five groups: sham group, I/R group, HT+I/R group, HT+LY294002+I/R group, and LY+I/R group. Myocardial inf...

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Main Authors: Ying-hao Pei, Jiao Chen, Liang Xie, Xiao-min Cai, Run-Hua Yang, Xing Wang, Jian-bin Gong
Format: Article
Language:English
Published: Wiley 2016-01-01
Series:Mediators of Inflammation
Online Access:http://dx.doi.org/10.1155/2016/1232103
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author Ying-hao Pei
Jiao Chen
Liang Xie
Xiao-min Cai
Run-Hua Yang
Xing Wang
Jian-bin Gong
author_facet Ying-hao Pei
Jiao Chen
Liang Xie
Xiao-min Cai
Run-Hua Yang
Xing Wang
Jian-bin Gong
author_sort Ying-hao Pei
collection DOAJ
description Objective. To investigate the effects and mechanisms of hydroxytyrosol (HT) during the pathogenesis of myocardial ischemia reperfusion (I/R) in rat hearts. Methods. The rats were randomized into five groups: sham group, I/R group, HT+I/R group, HT+LY294002+I/R group, and LY+I/R group. Myocardial infarct size, markers of oxidative stress, extent of myocardial apoptosis, echocardiographically assessed cardiac function, and expression of Akt and GSK 3β were measured in each group. Results. Prereperfusion administration of HT was associated with a significantly smaller area of myocardial infarction and remarkably decreased level of myocardial apoptosis and necrosis, as evidenced by a lower apoptotic index, reduced cleaved caspase-3, and the serum activities of lactate dehydrogenase and creatinine kinase MB. Moreover, HT also attenuated the impairment of cardiac systolic function. However, cotreatment with LY294002 and HT completely abolished the above cardioprotective effects of HT. A subsequent mechanistic study revealed that the cardioprotective effects of HT during the process of I/R of the myocardium were dependent on the activation of the Akt/GSK3β pathway. Conclusion. Pretreatment with HT may have antiapoptotic and cardioprotective effects against myocardial I/R injury, and these effects seem to be related to the activation of the Akt/GSK3β pathway in the myocardium.
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series Mediators of Inflammation
spelling doaj-art-ea1105a92c4645be9cfbfebb55d0c88d2025-02-03T01:26:07ZengWileyMediators of Inflammation0962-93511466-18612016-01-01201610.1155/2016/12321031232103Hydroxytyrosol Protects against Myocardial Ischemia/Reperfusion Injury through a PI3K/Akt-Dependent MechanismYing-hao Pei0Jiao Chen1Liang Xie2Xiao-min Cai3Run-Hua Yang4Xing Wang5Jian-bin Gong6Department of Intensive Care Unit, Jiangsu Provincial Hospital of Traditional Chinese Medicine, The Affiliated Hospital of Nanjing University of Traditional Chinese Medicine, 155 Han Zhong Road, Nanjing 210029, ChinaDepartment of Intensive Care Unit, Nanjing Integrated Traditional Chinese and Western Medicine Hospital, Nanjing University of Traditional Chinese Medicine, 179 Xiao Lin-Wei, Nanjing 210014, ChinaDepartment of Cardiology, Jinling Hospital, Nanjing University, School of Medicine, Nanjing 210002, ChinaDepartment of Cardiology, Jinling Hospital, Nanjing University, School of Medicine, Nanjing 210002, ChinaDepartment of Intensive Care Unit, Nanjing Integrated Traditional Chinese and Western Medicine Hospital, Nanjing University of Traditional Chinese Medicine, 179 Xiao Lin-Wei, Nanjing 210014, ChinaDepartment of Intensive Care Unit, Jiangsu Provincial Hospital of Traditional Chinese Medicine, The Affiliated Hospital of Nanjing University of Traditional Chinese Medicine, 155 Han Zhong Road, Nanjing 210029, ChinaDepartment of Cardiology, Jinling Hospital, Nanjing University, School of Medicine, Nanjing 210002, ChinaObjective. To investigate the effects and mechanisms of hydroxytyrosol (HT) during the pathogenesis of myocardial ischemia reperfusion (I/R) in rat hearts. Methods. The rats were randomized into five groups: sham group, I/R group, HT+I/R group, HT+LY294002+I/R group, and LY+I/R group. Myocardial infarct size, markers of oxidative stress, extent of myocardial apoptosis, echocardiographically assessed cardiac function, and expression of Akt and GSK 3β were measured in each group. Results. Prereperfusion administration of HT was associated with a significantly smaller area of myocardial infarction and remarkably decreased level of myocardial apoptosis and necrosis, as evidenced by a lower apoptotic index, reduced cleaved caspase-3, and the serum activities of lactate dehydrogenase and creatinine kinase MB. Moreover, HT also attenuated the impairment of cardiac systolic function. However, cotreatment with LY294002 and HT completely abolished the above cardioprotective effects of HT. A subsequent mechanistic study revealed that the cardioprotective effects of HT during the process of I/R of the myocardium were dependent on the activation of the Akt/GSK3β pathway. Conclusion. Pretreatment with HT may have antiapoptotic and cardioprotective effects against myocardial I/R injury, and these effects seem to be related to the activation of the Akt/GSK3β pathway in the myocardium.http://dx.doi.org/10.1155/2016/1232103
spellingShingle Ying-hao Pei
Jiao Chen
Liang Xie
Xiao-min Cai
Run-Hua Yang
Xing Wang
Jian-bin Gong
Hydroxytyrosol Protects against Myocardial Ischemia/Reperfusion Injury through a PI3K/Akt-Dependent Mechanism
Mediators of Inflammation
title Hydroxytyrosol Protects against Myocardial Ischemia/Reperfusion Injury through a PI3K/Akt-Dependent Mechanism
title_full Hydroxytyrosol Protects against Myocardial Ischemia/Reperfusion Injury through a PI3K/Akt-Dependent Mechanism
title_fullStr Hydroxytyrosol Protects against Myocardial Ischemia/Reperfusion Injury through a PI3K/Akt-Dependent Mechanism
title_full_unstemmed Hydroxytyrosol Protects against Myocardial Ischemia/Reperfusion Injury through a PI3K/Akt-Dependent Mechanism
title_short Hydroxytyrosol Protects against Myocardial Ischemia/Reperfusion Injury through a PI3K/Akt-Dependent Mechanism
title_sort hydroxytyrosol protects against myocardial ischemia reperfusion injury through a pi3k akt dependent mechanism
url http://dx.doi.org/10.1155/2016/1232103
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