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Melatonin regulates nitric oxide synthase expression in ischemic brain injury.

作者信息

Koh Phil-Ok

机构信息

Department of Anatomy, College of Veterinary Medicine, Research Institute of Life Science, Gyeongsang National University, 900 Gajwa-dong, Jinju, South Korea.

出版信息

J Vet Med Sci. 2008 Jul;70(7):747-50. doi: 10.1292/jvms.70.747.

DOI:10.1292/jvms.70.747
PMID:18685253
Abstract

Nitric oxide (NO) is produced by three NO synthases (NOS), iNOS, eNOS, and nNOS. Production of NO by iNOS plays key roles in neurodegeneration, while eNOS is a protective enzyme. This study investigated the neuroprotective effect of melatonin and the levels of NOS isoforms induced by melatonin in ischemic brain injury. Adult male rats were treated with melatonin (5 mg/kg) or vehicle prior to middle cerebral artery occlusion (MCAO). Brain samples were collected at 24 hr after the onset of occlusion. Results confirmed that melatonin significantly reduces infarct area. Western blot analysis was used to evaluate the expression levels of iNOS, eNOS, and nNOS. The level of iNOS and nNOS increased in vehicle-treated animals, while melatonin prevented injury-induced increase of iNOS. In contrast to iNOS levels, eNOS levels decreased in vehicle-treated animals, while melatonin prevented the injury-induced decrease of eNOS. This study provides further evidence that melatonin exerts neuroprotective effects, and the regulation of NOS isoforms by melatonin may contribute to the neuroprotective effects.

摘要

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