Erythropoietin increases glutathione peroxidase enzyme activity and decreases lipid peroxidation levels in hypoxic-ischemic brain injury in neonatal rats

Kumral A., Gonenc S., Acikgoz O., Sonmez A., Genc K., Yilmaz O., ...More

BIOLOGY OF THE NEONATE, vol.87, no.1, pp.15-18, 2005 (SCI-Expanded) identifier identifier identifier

  • Publication Type: Article / Article
  • Volume: 87 Issue: 1
  • Publication Date: 2005
  • Doi Number: 10.1159/000080490
  • Journal Name: BIOLOGY OF THE NEONATE
  • Journal Indexes: Science Citation Index Expanded (SCI-EXPANDED)
  • Page Numbers: pp.15-18
  • Keywords: erythropoietin, neonatal rat, hypoxic-ischemic brain injury, lipid peroxidation, oxidative stress, glutathione peroxidase, OXYGEN RADICALS, NITRIC-OXIDE, DAMAGE, NEUROPROTECTION, INHIBITION, MECHANISMS, MODEL
  • Dokuz Eylül University Affiliated: Yes

Abstract

Background: We have previously shown that erythropoietin (Epo) exerts neuroprotective effects in the Rice-Vannucci model of neonatal hypoxic-ischemic brain injury. However, the mechanisms of Epo protection in this model are still unclear. Objectives: In the present study, we studied the effects of systemically administered Epo on lipid peroxidation levels and antioxidant enzyme ( superoxide dismutase and glutathione peroxidase) activities following hypoxic-ischemic brain injury in neonatal rats. Methods: Seven-day-old Wistar rat pups were subjected to left carotid artery occlusion followed by 2.5 h of hypoxic exposure. Brain lipid peroxidation levels and antioxidant enzyme activities were measured in the injured hemispheres 24 h after the hypoxic-ischemic insult. Results: Hypoxic-ischemic injury significantly increased the thiobarbituric acid-reactive substance levels in the injured hemispheres as compared to the control group. In addition, glutathione peroxidase activity was significantly elevated in Epo-treated animals compared to saline-treated animals and the control group. Conclusions: These results suggest that Epo exerts neuroprotective effects against hypoxic-ischemic brain injury at least partially via the modulation of antioxidant enzyme activity. Copyright (C) 2005 S. Karger AG, Basel.