Research Article N-Acetylcysteine Restores Sevoflurane Postconditioning Cardioprotection against Myocardial Ischemia-Reperfusion Injury in Diabetic Rats Jiefu Lin, 1 Tingting Wang, 2,3 Yalan Li, 1 Mengxia Wang, 1 Haobo Li, 2 Michael G. Irwin, 2 and Zhengyuan Xia 2,4 1 Department of Anesthesiology, Te First Afliated Hospital of Jinan University, Guangzhou 510642, China 2 Department of Anesthesiology, Te University of Hong Kong, Pokfulam, Hong Kong 3 Department of Anesthesiology, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430022, China 4 Department of Anesthesiology, Afliated Hospital of Guangdong Medical College, Zhanjiang 524023, China Correspondence should be addressed to Yalan Li; tyalan@jnu.edu.cn and Zhengyuan Xia; zyxia@hku.hk Received 4 June 2015; Revised 30 July 2015; Accepted 26 August 2015 Academic Editor: Dake Qi Copyright © 2016 Jiefu Lin et al. Tis 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. Te efect of sevofurane postconditioning (sevo-postC) cardioprotection is compromised in diabetes which is associated with increased oxidative stress. We hypothesized that antioxidant N-Acetylcysteine may enhance or restore sevo-postC cardioprotection in diabetes. Control or streptozotocin-induced Type 1 diabetic rats were either untreated or treated with N-Acetylcysteine for four weeks starting at fve weeks afer streptozotocin injection and were subjected to myocardial ischemia-reperfusion injury (IRI), in the absence or presence of sevo-postC. Diabetes showed reduction of cardiac STAT3 activation (p-STAT3) and adiponectin with concomitantly increase of FoxO1 and CD36, which associated with reduced sevo-postC cardioprotection. N-Acetylcysteine and sevo-postC synergistically reduced the infarct size in diabetic groups. N-Acetylcysteine remarkably increased cardiac p-STAT3 which was further enhanced by sevo-postC. N-Acetylcysteine but not sevo-postC decreased myocardial FoxO1 while sevo-postC but not N-Acetylcysteine signifcantly increased myocardiac adiponectin in diabetic rats. It is concluded that late stage diabetic rats displayed reduction of cardiac p-STAT3, adiponectin defciency, and increase of FoxO1 and CD36 expression, which may be responsible for the loss of myocardial responsiveness to sevo-postC cardioprotection. N-Acetylcysteine restored Sevo-postC cardioprotection in diabetes possibly through enhancing cardiac p-STAT3 and adiponectin and reducing Fox1 and CD36. 1. Introduction Ischemic heart disease (IHD) is the main cause of morbidity and mortality in diabetes. Patients with diabetes are particu- larly at risk of perioperative myocardial infarction with con- sequent ischemia and reperfusion injury (IRI). Sevofurane postconditioning (sevo-postC) has been shown to attenuate myocardial IRI by restraining the adhesion of infammatory cells, blocking up free oxygen radicals, and preventing cal- cium overload [1]. However, the benefcial efect of sevo- PostC is markedly attenuated by diabetes and the underlying mechanism is unclear. Diabetes can cause impairments to both phosphatidylinositol 3-kinase- (PI3K-) Akt and Janus kinase (Jak-) STAT3, which are the two classic signaling pathways of myocardial protection mechanisms and thus obstruct the postconditioning of myocardium [2, 3]. Recent studies indicated that the inability of insulin to restore sevo- postC cardioprotection in diabetes might be attributed to diabetes-induced STAT3 mediated inhibition of PI3K signal- ing [4]. Interestingly, our previous study has demonstrated that antioxidant N-Acetylcysteine (NAC) can partially restore the activation of Akt and STAT3 and subsequently attenuated myocardial IRI in the early stage of diabetic rats [5, 6]. However, whether NAC can restore the cardioprotection of sevo-IPostC through the restoration of STAT3 mediated signaling remains unknown. Hindawi Publishing Corporation Journal of Diabetes Research Volume 2016, Article ID 9213034, 8 pages http://dx.doi.org/10.1155/2016/9213034