Melatonin and ischemia–reperfusion injury of the brain
Article first published online: 9 JAN 2008
© 2008 The Authors. Journal compilation © 2008 Blackwell Munksgaard
Journal of Pineal Research
Volume 45, Issue 1, pages 1–7, August 2008
How to Cite
Cervantes, M., Moralí, G. and Letechipía-Vallejo, G. (2008), Melatonin and ischemia–reperfusion injury of the brain. Journal of Pineal Research, 45: 1–7. doi: 10.1111/j.1600-079X.2007.00551.x
- Issue published online: 14 JUL 2008
- Article first published online: 9 JAN 2008
- Received October 20, 2007; accepted November 27, 2007.
- brain injury;
Abstract: This review summarizes the reports that have documented the neuroprotective effects of melatonin against ischemia/reperfusion brain injury. The studies were carried out on several species, using models of acute focal or global cerebral ischemia under different treatment schedules. The neuroprotective actions of melatonin were observed during critical evolving periods for cell processes of immediate or delayed neuronal death and brain injury, early after the ischemia/reperfusion episode. Late neural phenomena accounting either for brain damage or neuronal repair, plasticity and functional recovery taking place after ischemia/reperfusion have been rarely examined for the protective actions of melatonin. Special attention has been paid to the advantageous characteristics of melatonin as a neuroprotective drug: bioavailability into brain cells and cellular organelles targeted by morpho-functional derangement; effectiveness in exerting several neuroprotective actions, which can be amplified and prolonged by its metabolites, through direct and indirect antioxidant activity; prevention and reversal of mitochondrial malfunction, reducing inflammation, derangement of cytoskeleton organization, and pro-apoptotic cell signaling; lack of interference with thrombolytic and neuroprotective actions of other drugs; and an adequate safety profile. Thus, the immediate results of melatonin actions in reducing infarct volume, necrotic and apoptotic neuronal death, neurologic deficits, and in increasing the number of surviving neurons, may improve brain tissue preservation. The potential use of melatonin as a neuroprotective drug in clinical trials aimed to improve the outcome of patients suffering acute focal or global cerebral ischemia should be seriously considered.