Abstract
The development of isoproterenol- (ISO-) induced oxidative stress in the myocardium results in myocardial necrosis. Sulforaphane (SFN-0.4% of sulforaphane from standardized broccoli sprout extract) possesses chemoprotective, antidiabetic, and antibacterial activities and is also active against cardiovascular-related problems due to its antioxidant properties. This study was designed to investigate the cardioprotective effect of SFN against isoproterenol-induced myocardial injury in mice. Healthy male Swiss albino mice weighing 20–30 g were used in this study. These mice were randomly divided into five groups (n = 6). All the mice in the experimental groups received isoproterenol (5 mg/kg bw, via i.p.) consecutively for 2 days. The mice were treated with SFN (4 mg/kg bw) and α-tocopherol (TCF) (10 mg/kg bw) by oral gavage for 1-7 days as pre- and posttreatment for the prophylactic and treatment groups, respectively. On day 10, the following parameters were studied: heart weight to body weight ratio, antioxidant parameters, and cardiac markers; and mitochondrial enzymes were estimated for cardioprotection. Administration of isoproterenol in mice showed an increased level of serum cardiac markers and heart mitochondrial ATPase enzymes. An increased level of myocardial thiobarbituric acid-reactive substance and decreased levels of endogenous antioxidant enzymes indicated that oxidative stress is induced by isoproterenol in the myocardium. The administration of SFN in mice restored the levels of all biochemical parameters to near-normal levels. Histopathological studies further confirmed the protective effect of sulforaphane. This study concluded that treatment with SFN boosts the endogenous antioxidant activity and prevents isoproterenol-induced myocardial injury.
Highlights
Ischemic heart disease (IHD) is one of the leading causes of death with high mortality and morbidity rates worldwide [1]
Patients with IHD are prone to myocardial injury, which leads to myocardial dysfunction and myocardial ischemia [2]
This study showed that ISO-induced severe oxidative stress generates free radicals that stimulate lipid peroxidation and results in irreversible damage to the myocardial membrane
Summary
Ischemic heart disease (IHD) is one of the leading causes of death with high mortality and morbidity rates worldwide [1]. Several mechanisms were documented in the pathogenesis of IHD, excessive production of reactive oxygen species (ROS) was considered a prominent mechanism during myocardial ischemia [3, 4]. Reducing ROS during myocardial ischemic injury was considered the best treatment option [4]. Isoproterenol (ISO) is a synthetic -adrenergic agonist that leads to oxidative stress, causing significant myocardial injury. The development of oxidative stress through generation of free radicals has established pathogenesis mechanism for myocardial injury [3, 4]. The antioxidant potential of sulforaphane was well established and documented through several research [8, 9]. This study was carried out to determine the potential protective role of SFN through antioxidant and other protective mechanism against ISOinduced myocardial injury in mice as an animal model
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