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

被引：61

作者：

Di Pietro, Valentina ^{[1
]}

Lazzarino, Giacomo ^{[2
]}

Amorini, Angela Maria ^{[2
]}

Tavazzi, Barbara ^{[2
]}

D'Urso, Serafina ^{[3
]}

Longo, Salvatore ^{[2
]}

Vagnozzi, Roberto ^{[4
]}

Signoretti, Stefano ^{[5
]}

Clementi, Elisabetta ^{[6
]}

Giardina, Bruno ^{[2
]}

Lazzarino, Giuseppe ^{[3
]}

Belli, Antonio ^{[1
]}

机构：

[1] Univ Birmingham, Coll Med & Dent Sci, Sch Clin & Expt Med, Neurotrauma & Neurodegenerat Sect, Birmingham, W Midlands, England

[2] Univ Cattolica Sacro Cuore, Inst Biochem & Clin Biochem, Rome, Italy

[3] Univ Catania, Div Biochem & Mol Biol, Dept Biol Geol & Environm Sci, I-95125 Catania, Italy

[4] Univ Roma Tor Vergata, Neurosurg Sect, Dept Biomed & Prevent, Rome, Italy

[5] San Camillo Hosp, Div Neurosurg, Dept Neurosci Head & Neck Surg, Rome, Italy

[6] Univ Cattolica Sacro Cuore, CNR Inst Chim Riconoscimento Mol, Rome, Italy

来源：

FREE RADICAL BIOLOGY AND MEDICINE | 2014年 / 69卷

关键词：

Brain antioxidants; Neuroglobin; Neuroprotection; Nitrosative stress; Oxidative stress; Traumatic brain injury; Free radicals; OXYGEN-GLUCOSE DEPRIVATION; MOUSE CORTICAL-NEURONS; OXIDATIVE STRESS; GENE-EXPRESSION; IN-VITRO; MODEL; APOPTOSIS; SAMPLES; PATHOPHYSIOLOGY; NEUROPROTECTION;

D O I：

10.1016/j.freeradbiomed.2014.01.032

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

071010 ; 081704 ;

摘要：

Neuroglobin is a neuron-specific hexacoordinated globin capable of binding various ligands, including 02, 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.(c) 2014 The Authors. Published by Elsevier Inc

引用

页码：258 / 264

页数：7

共 56 条

[1] Induction of oxidative and nitrosative damage leads to cerebrovascular inflammation in an animal model of mild traumatic brain injury induced by primary blast [J].