Role of exogenous melatonin on adriamycin-induced changes in the rat heart
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.
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ABSTRACT: The review analyzed morphology, molecular and functional aspects of pineal gland aging and methods of it correction. The pineal gland is central organ, which regulates activity of neuroimmunoendocrine, antioxidant and other organisms systems. Functional activity of pineal gland is discreased at aging, which is the reason of melatonin level changing. The molecular and morphology research demonstrated, that pineal gland hadn't strongly pronounced atrophy at aging. Long-term experience showed, that peptides extract of pineal gland epithalamin and synthetic tetrapeptide on it base epithalon restored melatonin secretion in pineal gland and had strong regulatory activity at neuroimmunoendocrine and antioxidant organism systems.
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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.
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