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Journal of Biomedicine and Biotechnology
Volume 2011 (2011), Article ID 384627, 9 pages
http://dx.doi.org/10.1155/2011/384627
Research Article

Shen-Fu Injection Preconditioning Inhibits Myocardial Ischemia-Reperfusion Injury in Diabetic Rats: Activation of eNOS via the PI3K/Akt Pathway

1Department of Anesthesiology, Renmin Hospital of Wuhan University, Wuhan, Hubei 430060, China
2Department of Gastroenterology, Renmin Hospital of Wuhan University, Wuhan, Hubei 430060, China
3Department of Pharmacology, School of Medicine, Wuhan University, Donghu Road, Wuhan 430071, China
4Department of Cardiovascular Surgery, Renmin Hospital of Wuhan University, Wuhan, Hubei 430060, China

Received 19 August 2010; Accepted 22 October 2010

Academic Editor: Monica Fedele

Copyright © 2011 Yang Wu 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

The aim of this paper is to investigate whether Shen-fu injection (SFI), a traditional Chinese medicine, could attenuate myocardial ischemia-reperfusion (MI/R) injury in diabetes. Streptozotocin-induced diabetic rats were randomly assigned to the Sham, I/R, SFI preconditioning, and SFI plus wortmannin (a phosphatidylinositol 3-kinase inhibitor) groups. After the treatment, hearts were subjected to 30 min of coronary artery occlusion and 2 h reperfusion except the Sham group. Myocardial infarct size and cardiomyocytes apoptosis were increased significantly in MI/R group as compared with the Sham group. SFI preconditioning significantly decreased infarct size, apoptosis, caspase-3 protein expression, MDA level in myocardial tissues, and plasma level of CK and LDH but increased p-Akt, p-eNOS, bcl-2 protein expression, and SOD activity compared to I/R group. Moreover, SFI-induced cardioprotection was abolished by wortmannin. We conclude that SFI preconditioning protects diabetic hearts from I/R injury via PI3K/Akt-dependent pathway.