Abstract
BackgroundErythropoietin (EPO) and its covalently modified analogs are neuroprotective in various models of brain damage and disease. We investigated the effect on brain damage and memory performance, of a continuous 3-day intravenous infusion of EPO, starting 20 min after a transient 10 minute period of global cerebral ischemia in the rat.ResultsWe found no effect on selective neuronal damage in the CA1 region of the hippocampus, neocortical damage and damage to the striatum assessed at 7 days after ischemia. Also, no differences were observed in sensori-motor scores between EPO treated and saline treated ischemic animals. In contrast, memory performance was significantly improved in the EPO treated group. Saline treated injured animals (n = 7) failed in a test assessing recovery of spatial memory (6/6 and 5/6), while EPO treated animals had few and none failures (0/7 and 1/7).ConclusionWe conclude that although post-ischemic treatment with EPO is not neuroprotective in a model of cardiac arrest brain ischemia, its markedly positive effect on brain plasticity and recovery of memory function warrants consideration as treatment of cardiac arrest patients.
Highlights
Erythropoietin (EPO) and its covalently modified analogs are neuroprotective in various models of brain damage and disease
The EPO gene is regulated by hypoxia inducing factor (HIF), where it stimulates erythropeoisis and proliferation of parenchymal cells, by acting on the EPO receptor (EpoR) coupled to PI3-kinase, JAK/STAT and NF-κB pathways [4,5,6]
This study was conducted to investigate neuroprotective effects of EPO treatment in rats subjected to global ischemia and sought at identifying if the treatment is associated with an improvement of sensorimotor and memory function
Summary
Erythropoietin (EPO) and its covalently modified analogs are neuroprotective in various models of brain damage and disease. We investigated the effect on brain damage and memory performance, of a continuous 3-day intravenous infusion of EPO, starting 20 min after a transient 10 minute period of global cerebral ischemia in the rat. In models of global ischemia, mimicking cardiac arrest, EPO is protective though only if applied prior to or 20 minutes after ischemia and only when administered through the intracerebroventricular (i.c.v.) route [14]. The aim of the present investigation was to study the effect of EPO treatment as a continuous intravenous administration in a model of global ischemia starting the treatment 20 minutes after reperfusion. We employed the two vessel occlusion (2-VO) model of global cerebral ischemia [16] and assessed the histological outcome and sensori-motor and memory performance after ischemia
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