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Melatonin protects against isoproterenol-induced alterations in cardiac mitochondrial energy-metabolizing enzymes, apoptotic proteins, and assists in complete recovery from myocardial injury in rats.
Journal of Pineal Research ( IF 10.3 ) Pub Date : 2012-10-11 , DOI: 10.1111/j.1600-079x.2012.00984.x
Debasri Mukherjee 1 , Arnab K Ghosh , Arun Bandyopadhyay , Anjali Basu , Santanu Datta , Sanjib K Pattari , Russel J Reiter , Debasish Bandyopadhyay
Affiliation  

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and to test whether melatonin has a role in preventing myocardial injury and recovery when the ISO-induced stress is withdrawn.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.

中文翻译:

褪黑素可防止异丙肾上腺素引起的心脏线粒体能量代谢酶,凋亡蛋白的改变,并帮助大鼠从心肌损伤中完全恢复。

进行本研究以探讨褪黑素对酒石酸异丙肾上腺素(ISO)诱导的大鼠心肌的保护作用,并测试褪黑素是否在消除ISO诱导的应激时具有预防心肌损伤和恢复的作用。用ISO进行的大鼠治疗改变了一些与能量代谢有关的关键线粒体酶的活性,某些应​​激蛋白的水平以及与细胞凋亡有关的蛋白。当以10 mg / kg BW的剂量对动物进行褪黑素预处理时,发现这些变化得到了改善。ip除了能够减轻ISO诱导的线粒体功能障碍外,我们还研究了褪黑素在恢复线粒体中的作用。 ISO引起的心脏组织损伤。发现停用ISO治疗后继续褪黑激素治疗可降低心脏损伤生物标志物的活性,包括血清谷氨酸草酰乙酸转氨酶(SGOT),乳酸脱氢酶(LDH)和心脏特异性LDH1,以控制水平。通过继续褪黑激素治疗,组织脂质过氧化和还原型谷胱甘肽的水平也恢复到对照动物体内的水平。在ISO后治疗期间继续褪黑激素治疗也可以改善心脏组织形态和心脏功能。因此,这些发现表明褪黑素以低药理剂量提供心脏保护的能力及其在恢复过程中的作用。褪黑激素是一种毒性极低或无毒性的分子,可以被认为是治疗缺血性心脏病的一种疗法。
更新日期:2012-03-12
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