Role of exogenous melatonin on adriamycin-induced changes in the rat heart

ArticleinEuropean review for medical and pharmacological sciences 14(5):435-41 · May 2010with5 Reads
Source: PubMed
The protective effect of melatonin on adriamycin (ADM)-induced cardiotoxicity was investigated in the rat heart. Melatonin is a pineal hormone with free radical scavenging activity on oxidants; therefore it may decrease the ADM-induced oxidative stress and cardiotoxicity so that therapeutic efficacy might be enhanced. Wistar rats in 4 groups were treated with saline (control), melatonin (MEL), adriamycin (ADM) and melatonin plus adriamycin (MEL+ADM). Adriamycin given at a single dose of 15 mg/kg significantly increased lipid peroxidation products as measured by thiobarbituric acid reactive substances (TBARS). Melatonin (5 mg/kg bw) given 2 days before and 7 days after ADM treatment reduced TBARS level. Adriamycin significantly reduced superoxide dismutase activity which was elevated by melatonin treatment. Additionally, ADM significantly increased catalase enzyme activity while melatonin normalized the ADM induced alteration in activity of catalase. The combined use of ADM and melatonin reduces the threat of cardiomyopathy. Melatonin seems to hold promise as a therapeutic treatment and can be recommended as an adjunct in antitumor therapy as a safe and effective protection against acute ADM-induced cardiotoxicity.
    • "Correlation between the increase in the maximal concentration of melatonin and total antioxii dant status during nighttime is one more proof of the antioxidant effect of MT [25]. It was shown that MT participates in the regulation of the cardiovascular system [26]. Administration of MT by elderly persons with a decreased function of the PG resulted in normalization of blood pressure and a decrease in the frequency of heart contractions and an increase in the variability of the heart rhythm [5, 27]. "
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  • [Show abstract] [Hide abstract] ABSTRACT: This study aimed to observe the influence of intermittent hypoxia on rat INS-1 cells and the protective effect of melatonin (MT). Intermittent hypoxia condition was induced in rat INS-1 cells. The supernatants were used to detect oxidative stress indicators, and the cells were used to detect JNK1 mRNA and JNK1/2 protein. After different dose-dependent interventions of MT, the cells were harvested to observe corresponding oxidative stress indicators and JNK1/2 protein change. With prolonged exposure time, malondialdehyde (MDA) increased in cultured supernatants whereas superoxide dismutase (SOD) activity decreased. Cells with intermittent hypoxia showed significantly increased JNK1 mRNA expression, whereas phosphorylated JNK1 was highly expressed on the third day. With increased MT dose, MDA in cultured supernatants decreased whereas SOD activity increased. In the group dosed with 100 µM MT, phosphorylated JNK1 protein expression significantly decreased. Intermittent hypoxia can cause oxidative damage to INS-1 cells possibly by increasing the JNK1 transcription level and protein activation. A high dose of MT (100 µM) can protect INS-1 cells from oxidative damage induced by intermittent hypoxia.
    Article · Apr 2014
    W LuW LuL LiuL LiuH LiH Li+4 more authors ...J KangJ Kang

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