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.