Melatonin protects against isoproterenol‐induced alterations in cardiac mitochondrial energy‐metabolizing enzymes, apoptotic proteins, and assists in complete recovery from myocardial injury in rats

Abstract

The present study was undertaken to explore the protective effect of melatonin against isoproterenol bitartrate (ISO)-induced rat myocardial injury and to test whether melatonin has a role in preventing myocardial injury and recovery when the ISO-induced stress is withdrawn. Treatment for rats with ISO altered the activities of some of the key mitochondrial enzymes related to energy metabolism, the levels of some stress proteins, and the proteins related to apoptosis. These changes were found to be ameliorated when the animals were pretreated with melatonin at a dose of 10 mg/kg BW, i.p. In addition to its ability to reduce ISO-induced mitochondrial dysfunction, we also studied the role of melatonin in the recovery of the cardiac tissue after ISO-induced damage. Continuation of melatonin treatment in rats after the withdrawal of ISO treatment was found to reduce the activities of cardiac injury biomarkers including serum glutamate oxaloacetate transaminase (SGOT), lactate dehydrogenase (LDH), and cardio-specific LDH1 to control levels. The levels of tissue lipid peroxidation and reduced glutathione were also brought back to that seen in control animals by continued melatonin treatment. Continuation of melatonin treatment in post-ISO treatment period was also found to improve cardiac tissue morphology and heart function. Thus, the findings indicate melatonin’s ability to provide cardio protection at a low pharmacological dose and its role in the recovery process. Melatonin, a molecule with very low or no toxicity may be considered as a therapeutic for the treatment for ischemic heart disease.

Melatonin reduces cardiac remodeling and improves survival in rats with isoproterenol‐induced heart failure

“…The SBP decline was partly prevented by melatonin indicating preservation of the systolic LV function. This is in agreement with findings of other authors that melatonin improved the systolic or diastolic function in isoproterenol‐damaged heart . Thus, it seems that although hypertrophy of the LV is not reduced by melatonin, this molecule modifies LV structure in terms of the shift from pathological LVH to more physiological hypertrophy.…”

N-Acetyl-Serotonin Protects HepG2 Cells from Oxidative Stress Injury Induced by Hydrogen Peroxide

“…Through a variety of studies, we know that oxidants can not only stimulate inflammatory cytokine such as interleukin-8 [37, 82] in HepG2 cells and cause cellular senescence [83], but also induce apoptosis in HepG2 cells, [37]; certain apoptotic agents increase the production of ROS in mitochondria [84], and antioxidants such as N-acetylcysteine [85, 86], melatonin [87, 88], NAS [26], and Vitamin E [27] can prevent apoptosis. Such studies also confirmed the association between ROS-apoptosis.…”

A review of melatonin as a suitable antioxidant against myocardial ischemia–reperfusion injury and clinical heart diseases

“…Moreover, numerous studies suggest that melatonin plays a significant role in hypertension [24,25], heart failure [12,26], drug-induced myocardial injury [27,28], and atherosclerosis [29,30]. A large amount of data published by a variety of investigations has demonstrated that melatonin can effectively reduce myocardial IR injury (Table 1).…”