Research Article Thymoquinone Protects against Myocardial Ischemic Injury by Mitigating Oxidative Stress and Inflammation Shreesh Ojha, 1 Sheikh Azimullah, 1 Rajesh Mohanraj, 1 Charu Sharma, 2 Javed Yasin, 2 Dharamvir S. Arya, 3 and Abdu Adem 1 1 Department of Pharmacology and Terapeutics, College of Medicine and Health Sciences, United Arab Emirates University, P.O. Box 17666, Al Ain, Abu Dhabi, UAE 2 Department of Internal Medicine, College of Medicine and Health Sciences, United Arab Emirates University, P.O. Box 17666, Al Ain, Abu Dhabi, UAE 3 Department of Pharmacology, All India Institute of Medical Sciences, New Delhi 29, India Correspondence should be addressed to Shreesh Ojha; shreeshojha@uaeu.ac.ae Received 5 December 2014; Accepted 21 February 2015 Academic Editor: Muhammad N. Ghayur Copyright © 2015 Shreesh Ojha 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 present study was aimed at investigating the cardioprotective activity of thymoquinone (TMQ), an active principle of the herb, Nigella sativa, which is used for the management of various diseases. Te present study examined the cardioprotective efect of TMQ in isoproterenol- (ISP-) induced myocardial infarction in rats. Myocardial infarction was induced by two subcutaneous injections of ISP (85 mg/kg) at an interval of 24 hr. TMQ (20 mg/kg) was administered orally for 21 days. ISP-treated rats showed depletion of antioxidants and marker enzymes from myocardium along with lipid peroxidation and enhanced levels of proinfammatory cytokines. ISP also induced histopathological alterations in myocardium. Treatment with TMQ prevented the depletion of endogenous antioxidants and myocyte injury marker enzymes and inhibited lipid peroxidation as well as reducing the levels of proinfammatory cytokines. TMQ pretreatment also reduced myonecrosis, edema, and infltration of infammatory cells and showed preservation of cardiomyocytes histoarchitecture. Te present study results demonstrate that TMQ exerts cardioprotective efect by mitigating oxidative stress, augmenting endogenous antioxidants, and maintaining structural integrity. Te results of the present study indicate that TMQ may serve as an excellent agent alone or as adjuvant to prevent the onset and progression of myocardial injury. 1. Introduction Myocardial infarction (MI) is a major form of ischemic heart disease, characterized by an imbalance of coronary blood supply and myocardial demand which results in ischemia and myocardial death. Experimental and clinical studies have shown that, during ischemic injury, produced oxidative stress plays a key role in the development of MI [1, 2]. In ischemic tissues, the oxygen-free radicals have been implicated in oxidative chain reactions, which damage the cell membrane and subcellular structures containing phospholipids and proteins. Tese reactions further cause phospholipid perox- idation and subsequently lead to functional, structural, and metabolic alterations in the heart [2]. A large number of epidemiological, clinical, and experi- mental studies have demonstrated that the use of antioxidants as a preventive approach may limit the infarct size and atten- uate myocardial dysfunction as well as slowing down the progression and consequences of MI [3–6]. Antioxidants not only suppress the formation of reactive oxygen species (ROS) and free radical generation and or augmentation of endoge- nous antioxidant enzymes but also modulate heart function [2–4]. Te central role of ROS in the pathophysiology of MI has been confrmed by the ability of antioxidants to reduce ischemic injury in the animal model of isoproterenol- (ISP-) induced MI [7–9]. Te pathophysiological and morphologi- cal changes in myocardium of ISP administered to rats closely resemble human MI [7, 8]. ISP, a synthetic catecholamine and Hindawi Publishing Corporation Evidence-Based Complementary and Alternative Medicine Volume 2015, Article ID 143629, 12 pages http://dx.doi.org/10.1155/2015/143629