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Department of Psychiatry, Western Psychiatric Institute and Clinic, University of Pittsburgh School of Medicine, Pennsylvania, USA.
The inflammatory response following mechanical brain injury is characterized by an increase in the cytokine interleukin-1 beta (IL-1 beta) followed by a large elevation in the neurotrophin, nerve growth factor (NGF). The substantial upregulation in NGF observed in our previous studies suggests that it may have functions in addition to that of a target-derived neuronal support mechanism. We hypothesize that NGF is a mediator of oxidative homeostasis, by inducing the production of oxygen-free radical scavengers in brain tissue following injury. We tested this hypothesis by measuring the activity of the antioxidant enzymes, glutathione peroxidase (GSH-Px), and catalase in cortical brain tissue following experimentally induced cortical contusion. We observed a twofold increase in GSH-Px and a threefold increase in catalase activities in a time course which reflected the temporal increase in NGF observed following the same cortical contusion model. These findings support the hypothesis and illuminate an important reparative role for NGF following trauma.
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