Neuroprotective effect of melatonin: a novel therapy against perinatal hypoxia-ischemia

Abstract

One of the most common causes of mortality and morbidity in children is perinatal hypoxia-ischemia (HI). In spite of the advances in neonatology, its incidence is not diminishing, generating a pediatric population that will require an extended amount of chronic care throughout their lifetime. For this reason, new and more effective neuroprotective strategies are urgently required, in order to minimize as much as possible the neurological consequences of this encephalopathy. In this sense, interest has grown in the neuroprotective possibilities of melatonin, as this hormone may help to maintain cell survival through the modulation of a wide range of physiological functions. Although some of the mechanisms by which melatonin is neuroprotective after neonatal asphyxia remain a subject of investigation, this review tries to summarize some of the most recent advances related with its use as a therapeutic drug against perinatal hypoxic-ischemic brain injury, supporting the high interest in this indoleamine as a future feasible strategy for cerebral asphyctic events.

Figure 1

Nissl-stained (A–C), myelin basic protein (D–F) and glial fibrillary acidic protein (G–I) immunolabeled brain sections corresponding to the surrounding areas of the CA1 region of the hippocampus and the external capsule showing cell loss (B), myelination deficit (E) and reactive gliosis (H) after hypoxia-ischemia and recovery after melatonin administration. Seven-day old rats were subjected to hypoxia-ischemia (left common carotid artery ligated and then 8% oxygen for 2 h) and sacrificed seven days after the injury. Pups without ischemia or hypoxia served as controls (Sham group). Bar: 100 μm.