Ergosterol Attenuates Isoproterenol-Induced Myocardial Cardiotoxicity
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Ergosterol Attenuates Isoproterenol‑Induced Myocardial Cardiotoxicity Qifei Xie1 · Suiji Li1 · Yun Gao2 · Ling Jin2 · Cuilian Dai1 · Juan Song1
© Springer Science+Business Media, LLC, part of Springer Nature 2020
Abstract Phytomedicine has shown a promising potential for the prevention of cardiovascular system diseases and disorders. This study aimed to evaluate protective effect of ergosterol (ER) on isoproterenol (ISO)-induced myocardial cardiotoxicity. We found that pretreatment with ER significantly decreased levels of myocardial CK-MB and LDH, and alleviated myocardial damage induced by ISO in rat model. In addition, ER restored Nrf2 and HO-1 expression and inhibited apoptosis through upregulating Bcl-2 and downregulating Bax, cytochrome c, cleaved caspase-3, caspase-9, and PARP in rat hearts. Hypoxiareoxygenation model in H9C2 cells confirmed the cardioprotective effects of ER. In conclusion, we provide both in vitro and in vivo evidence that ER significantly enhances Nrf2-mediated anti-oxidative activities, and exerts a protective effect on cardiomyocyte apoptosis. ER could be considered as a potential therapeutic agent to prevent myocardial injury. Keywords Ergosterol · Isoproterenol · Apoptosis · Oxidative stress · Myocardial injury
Introduction Myocardial infarction (MI) is a leading cause of death and disability worldwide. MI refers to a condition that myocardium suffers from irreversible damages caused by hypoxia–ischemia for a certain time followed by reperfusion [1]. In this process, ischemia of the myocardium causes excess generations of free radicals, which may induce oxidative and apoptotic damages [2]. Oxidative stress and inflammatory cytokines play important role in myocardial damage following acute myocardial infarction [3]. Currently, reperfusion is a standard therapy for MI, but it may lead to cardiomyocyte dysfunction known as ischemic reperfusion injury (IRI) [4]. Recent evidence suggests that oxidative stress, Handling Editor: Y. James Kang. * Cuilian Dai [email protected] * Juan Song [email protected] 1
Xiamen Cardiovascular Hospital, Xiamen University, Xiamen 361004, China
Department of Pathology, The Affiliated Kunshan Hospital of Jiangsu University, The First People’s Hospital of Kunshan, Suzhou 215300, China
2
inflammation and neurohumoral activation contribute to IRI [5]. In particular, adrenergic overstimulation-induced production of catecholamines plays a major role during stressinduced cardiac dysfunction [2]. The supraphysiological level of plasma catecholamines perturbs lipid metabolism in the heart and causes cardiomyocyte apoptosis or necrosis, resulting in serious myocardial damage [6]. Isoproterenol (ISO) is a β-adrenergic agonist and synthetic catecholamine that could induce myocardial lesions in rodents. ISO exposure induces severe stress to cardiomyocyte, which can lead to the loss of myocardial integrity through oxygen deficit, calcium overload, and free radical overproduction [2]. Oxidative stress has been recognized as a hallmark of myocardial injury
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