Comment on the Paper Entitled ‘Erythropoietin Ameliorates Oxidative Stress and Tissue Injury following Renal Ischemia/Reperfusion in Rat Kidney and Lung’
ing the free iron and reducing the oxidative brain injury. Thus, it improves the long-term brain healing after an insult by providing an increased oxygen-carrying capacity through erythropoiesis and angiogenesis and by increasing neurogenesis. The net effect of the acute actions of Epo is a decrease in apoptosis. Schelshorn et al . [5] found that neurons could specifically express hemoglobin in response to either hypoxia or Epo, and that neuronal hemoglobin expression may be neuroprotective by facilitating oxygen uptake in neurons and serving as an oxygen capacitator molecule. Furthermore, it has been demonstrated that the combined use of hypothermia and Epo has more expressed neuroprotective effects than the sole use of hypothermia after perinatal asphyxia in newborns [3] . We therefore recommend that Epo be included in the treatment guidelines as an adjunctive therapy to therapeutic hypothermia for neuroprotection following a hypoxic-ischemic insult in newborn infants.