Role of neotrofin in experimental hypoxic ischemic encephalopathy model

Hypoxia-ischemia is a major cause of perinatal brain injury in the newborn, leading to death or lifelong sequel such as cerebral palsy, mental retardation, learning disability and epilepsy. Despite developments in cardiopulmonary resuscitation, nursing and ventilation techniques, it still continues to be the most important cause of neurological morbidity and mortality. Regeneration ability of nerve tissue is limited. However, it is known that a group of agents called as neurotrophin released from brain tissue plays an important role in cell reproduction and regeneration. We also aimed at investigating effects of neotrofin, a nerve neurotophic factor agonist, on central nervous system in hypoxic-ischemic encephalopathy model. Therefore, hypoxic-ischemic brain injury model was formed in 21 Wistar-albino rat pups at their postnatal 7th day and intraperitoneal neotrofin was applied to treatment group. We found that neotrofin attenuates hypoxia-ischemia induced with neuronal density of hippocampus, prefrontal and parietal cortex, decreased apoptotic cell index in the same regions in this experimental study. These data suggest that a 60 mg/kg single dose of neotrofin can produce neuroprotective and anti-apoptotic effects in the neonatal hypoxic-ischemic brain. This is the first experimental demonstration that has shown the effects of neotrofin in the newborn rat brain. Given our results, neotrofin may be useful in reducing brain injury and possessing clinical relevance for the treatment of hypoxic-ischemic encephalopathy in the newborn.