Neuroglobin expression and oxidant/antioxidant balance after graded traumatic brain injury in the rat

Research output: Contribution to journalArticle

Authors

  • Giacomo Lazzarino
  • Angela Maria Amorini
  • Barbara Tavazzi
  • Serafina D'urso
  • Salvatore Longo
  • Roberto Vagnozzi
  • Stefano Signoretti
  • Elisabetta Clementi
  • Bruno Giardina
  • Giuseppe Lazzarino

Colleges, School and Institutes

External organisations

  • University of Catania
  • Catholic University of Rome
  • University of Rome Tor Vergata
  • S. Camillo Hospital

Abstract

Neuroglobin is a neuron-specific hexacoordinated globin capable of binding various ligands, including O2, NO, and CO, the biological function of which is still uncertain. Various studies seem to indicate that neuroglobin is a neuroprotective agent when overexpressed, acting as a potent inhibitor of oxidative and nitrosative stress. In this study, we evaluated the pathophysiological response of the neuroglobin gene and protein expression in the cerebral tissue of rats sustaining traumatic brain injury of differing severity, while simultaneously measuring the oxidant/antioxidant balance. Two levels of trauma (mild and severe) were induced in anesthetized animals using the weight-drop model of diffuse axonal injury. Rats were then sacrificed at 6, 12, 24, 48, and 120 h after traumatic brain injury, and the gene and protein expression of neuroglobin and the concentrations of malondialdehyde (as a parameter representative of reactive oxygen species-mediated damage), nitrite + nitrate (indicative of NO metabolism), ascorbate, and glutathione (GSH) were determined in the brain tissue. Results indicated that mild traumatic brain injury, although causing a reversible increase in oxidative/nitrosative stress (increase in malondialdehyde and nitrite + nitrate) and an imbalance in antioxidants (decrease in ascorbate and GSH), did not induce any change in neuroglobin. Conversely, severe traumatic brain injury caused an over nine- and a fivefold increase in neuroglobin gene and protein expression, respectively, as well as a remarkable increase in oxidative/nitrosative stress and depletion of antioxidants. The results of this study, showing a lack of effect in mild traumatic brain injury as well as asynchronous time course changes in neuroglobin expression, oxidative/nitrosative stress, and antioxidants in severe traumatic brain injury, do not seem to support the role of neuroglobin as an endogenous neuroprotective antioxidant agent, at least under pathophysiological conditions.

Details

Original languageEnglish
Pages (from-to)258-264
Number of pages7
JournalFree Radical Biology and Medicine
Volume69
Early online date31 Jan 2014
Publication statusPublished - 1 Apr 2014

Keywords

  • Brain antioxidants, Neuroglobin, Neuroprotection, Nitrosative stress, Oxidative stress, Traumatic brain injury, Free radicals

ASJC Scopus subject areas