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Mediators of Inflammation
Volume 2016, Article ID 1232103, 9 pages
http://dx.doi.org/10.1155/2016/1232103
Research Article

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

1Department 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, China
2Department of Intensive Care Unit, Nanjing Integrated Traditional Chinese and Western Medicine Hospital, Nanjing University of Traditional Chinese Medicine, 179 Xiao Lin-Wei, Nanjing 210014, China
3Department of Cardiology, Jinling Hospital, Nanjing University, School of Medicine, Nanjing 210002, China

Received 31 October 2015; Accepted 12 January 2016

Academic Editor: Tânia Silvia Fröde

Copyright © 2016 Ying-hao Pei 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

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.