Abstract
BackgroundThe neurohormone melatonin may prevent neuronal cell death caused by neurodegenerative diseases. Purpose: Using a transient cerebral ischemic model (MCAO), we assessed the neuroprotective effect of melatonin in an ischemic region. Results: In this study of efficacy, experimental animals were subjected to MCAO for 60 min, and then given melatonin (injected at 5 mg/kg). The following three groups were formed: (1) control group (MCAO vehicle); (2) melatonin pre‐treatment group (injected intraperitoneally 5 min prior to MCAO and again 1 h post‐occlusion); and, (3) melatonin post‐treatment group (injected subcutaneously [twice daily] post‐MCAO onset for 3 days). In melatonin‐treated ischemic rats, brain infarction was reduced 3 days post‐MCAO surgery compared with controls, and physiological and neurological features differed, including molecular changes associated with cell death. Significant decreases in p53, Bax, caspase‐6, and LC3 expression levels were observed in the melatonin pre‐ and post‐treatment groups (P < 0.05). Suggestion: The brain morphological and molecular changes indicate that melatonin is associated with neurogenesis and confers protection against neuronal cell death.Funding: 2012R1A1A2005089, 2013R1A2A2A01067169, KGM4611512, 2014R1A1A3051724
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