Erythropoietin prevents ischemia-reperfusion from inducing oxidative damage in fetal rat brain

Childs Nerv Syst. 2003 Jan;19(1):19-22. doi: 10.1007/s00381-002-0680-2. Epub 2002 Dec 14.

Abstract

Objective: The aim of this study was to show the effect of erythropoietin on ischemia-reperfusion-induced oxidative damage in fetal rat brain.

Methods: Fetal brain ischemia was induced by clamping the utero-ovarian artery bilaterally for 20 min, and reperfusion was achieved by removing the clamps for 30 min. The control group was made up of non-injured rats that were 19 days pregnant. In the ischemia-reperfusion group no treatment was given, while 0.4 ml of human serum albumin solution and 5,000 U/kg recombinant human erythropoietin (r-Hu-EPO) were administered in the vehicle and treatment groups 30 min before ischemia-reperfusion injury. Lipid peroxidation in the brain tissue was determined as the concentration of thiobarbituric acid-reactive substances (TBARS) for each fetal rat. A one-way analysis of variance and the post-hoc test were used for statistical analysis.

Results: TBARS increased to statistically significantly higher levels in fetal rat brain after ischemia-reperfusion injury than were found in the control group. Recombinant human erythropoietin prevented the increase in TBARS after ischemia-reperfusion injury.

Conclusion: Recombinant human erythropoietin has been shown to have neuroprotective effect in intrauterine ischemia-reperfusion-induced fetal brain damage in rats.

Publication types

  • Comparative Study

MeSH terms

  • Animals
  • Brain / blood supply
  • Brain / drug effects*
  • Brain / embryology
  • Brain / metabolism*
  • Erythropoietin / pharmacology*
  • Female
  • Humans
  • Lipid Peroxidation / drug effects
  • Oxidation-Reduction
  • Random Allocation
  • Rats
  • Rats, Wistar
  • Recombinant Proteins
  • Reperfusion Injury / metabolism
  • Reperfusion Injury / prevention & control*

Substances

  • Recombinant Proteins
  • Erythropoietin