Neuroglobin-overexpression reduces traumatic brain lesion size in mice
1 Departments of Orthopedic and Neurosurgery, The First Bethune Hospital of Jilin University, Changchun, Jilin, China
2 Neuroprotection Research Laboratory, Departments of Neurology and Radiology, Massachusetts General Hospital, Harvard Medical School, Charlestown, MA, USA
3 Department of Pediatrics, Pediatric Critical Care Medicine, Massachusetts General Hospital, Harvard Medical School, Charlestown, MA, USA
4 Neuroprotection Research Laboratory, Departments of Neurology and Radiology, Massachusetts General Hospital, 149 13th Street, Room 2401, Charlestown, MA, 02129, USA
Citation and License
BMC Neuroscience 2012, 13:67 doi:10.1186/1471-2202-13-67Published: 15 June 2012
Accumulating evidence has demonstrated that over-expression of Neuroglobin (Ngb) is neuroprotective against hypoxic/ischemic brain injuries. In this study we tested the neuroprotective effects of Ngb over-expression against traumatic brain injury (TBI) in mice.
Both Ngb over-expression transgenic (Ngb-Tg) and wild-type (WT) control mice were subjected to TBI induced by a controlled cortical impact (CCI) device. TBI significantly increased Ngb expression in the brains of both WT and Ngb-Tg mice, but Ngb-Tg mice had significantly higher Ngb protein levels at the pre-injury baseline and post-TBI. Production of oxidative tissue damage biomarker 3NT in the brain was significantly reduced in Ngb-Tg mice compared to WT controls at 6 hours after TBI. The traumatic brain lesion volume was significantly reduced in Ngb Tg mice compared to WT mice at 3 weeks after TBI; however, there were no significant differences in the recovery of sensorimotor and spatial memory functional deficits between Ngb-Tg and WT control mice for up to 3 weeks after TBI.
Ngb over-expression reduced traumatic lesion volume, which might partially be achieved by decreasing oxidative stress.