Hyperglycemia-Induced Inhibition of DJ-1 Expression Compromised the Effectiveness of Ischemic Postconditioning Cardioprotection in RatsReport as inadecuate




Hyperglycemia-Induced Inhibition of DJ-1 Expression Compromised the Effectiveness of Ischemic Postconditioning Cardioprotection in Rats - Download this document for free, or read online. Document in PDF available to download.

Oxidative Medicine and Cellular LongevityVolume 2013 2013, Article ID 564902, 8 pages

Research Article

Department of Anesthesiology, Renmin Hospital of Wuhan University, 99 Zi Yang Road, Wuhan, Hubei 430060, China

Department of Anesthesiology, The First Affiliated Hospital of University of South China, 69 Chuan Shan Road, Hengyang, Hunan 421001, China

Department of Cardiac Surgery, Chongqing Zhongshan Hospital, 312 Zhongshan Road, Chongqing 400013, China

Department of Anesthesiology, The University of Hong Kong, Hong Kong

Department of Anesthesiology, Affiliated Hospital of Guangdong Medical College, Zhanjiang, Guangdong 524001, China

Received 29 July 2013; Accepted 15 September 2013

Academic Editor: Qian Fan

Copyright © 2013 Min Liu 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

Ischemia postconditioning IpostC is an effective way to alleviate ischemia and reperfusion injury; however, the protective effects seem to be impaired in candidates with diabetes mellitus. To gain deep insight into this phenomenon, we explored the role of DJ-1, a novel oncogene, that may exhibit powerful antioxidant capacity in postconditioning cardioprotection in a rat model of myocardial ischemia reperfusion injury. Compared with normal group, cardiac DJ-1 was downregulated in diabetes. Larger postischemic infarct size as well as exaggeration of oxidative stress was observed, while IpostC reversed the above changes in normal but not in diabetic rats. DJ-1 was increased after ischemia and postconditioning contributed to a further elevation; however, no alteration of DJ-1 was documented in all subgroups of diabetic rats. Alteration of the cardioprotective PI3K-Akt signaling proteins may be responsible for the ineffectiveness of postconditioning in diabetes. There is a positive correlation relationship between p-Akt and DJ-1 but a negative correlation between infarct size and DJ-1, which may partially explain the interaction of DJ-1 and IpostC cardioprotection. Our result indicates a beneficial role of DJ-1 in myocardial ischemia reperfusion. Downregulation of cardiac DJ-1 may be responsible for the compromised diabetic heart responsiveness to IpostC cardioprotection.





Author: Min Liu, Bin Zhou, Zhong-Yuan Xia, Bo Zhao, Shao-Qing Lei, Qing-Jun Yang, Rui Xue, Yan Leng, Jin-Jin Xu, and Zhengyuan Xi

Source: https://www.hindawi.com/



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