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    The effect of melatonin on spinal cord after ischemia in rats
    (Nature Publishing Group, 2016) Aydemir, S.; Dogan, D.; Kocak, A.; Dilsiz, N.
    Study design: Experimental animal model to assess ischemic spinal cord injury (SCI) following occlusion of the thoracoabdominal aorta. Objectives: In the present study, we aimed to investigate the role of melatonin on SCI induced by ischemia and following reperfusion. Setting: Animal Research Laboratory, Inonu University, Malatya, Turkey. Methods: We evaluated oxidative damage and caspase-3 activity. In total, 32 adult Wistar albino rats were divided into four groups: Group 1, control (n=8); Group 2 (n=8), those subjected to ischemia/reperfusion (IR) by clamping the thoraco-abdominal aorta; Group 3 (n=8), melatonin (50 mg kg(-1)) treated; and Group 4 (n=8), melatonin (50 mg kg(-1)) followed by ischemia. All animals were kept alive for 48 h, and then spinal cord samples were removed. We assayed oxidative damage by measuring malondialdehyde (MDA), apoptosis by measuring activated caspase-3 (using immunoblots) and intrinsic antioxidative capacity by measuring reduced glutathione (GSH) levels in the spinal cord. Results: The results indicated a significant decrease in activity of caspase-3 in SCI animals after treatment with melatonin, as it significantly decreased the formation of MDA and decelerated the loss of GSH. Conclusion: This study suggested that melatonin could be an effective neuroprotective agent for treatment of SCI.
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    Role of exogenous melatonin on adriamycin-induced changes in the rat heart
    (Verduci Publisher, 2010) Aydemir, S.; Ozdemir, I.; Kart, A.
    Aim: 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. Materials and Methods: Wistar rats in 4 groups were treated with saline (control), melatonin (MEL), adriamycin (ADM) and melatonin plus adriamycin (MEL+ADM). Results: 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. Conclusions: 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.