Intracranial hemorrhage is one of the most common consequences of traumatic brain injury (TBI). The release of iron from the breakdown of hemoglobin during intracerebral hematoma resolution results in an increase in perihematomal non-heme iron. Lipocalin 2 (LCN-2) is a siderophore-binding protein that mediates transferrin-independent iron transport. This study examined the effects of TBI (lateral fluid percussion) on LCN-2 expression in Sprague-Dawley rats. LCN-2 protein levels were markedly increased in the ipsilateral cortex and hippocampus after TBI, with the highest level at day 1. Most LCN-2-positive cells appeared to be astrocytes. Treatment with an iron chelator, deferoxamine (100 mg/kg, intramuscularly), attenuated the TBI-induced upregulation of LCN-2. In summary, TBI resulted in upregulation of LCN-2 and deferoxamine reduced TBI-induced LCN-2 increase, suggesting LCN-2 may have a role in iron-trafficking after TBI.
Keywords: Deferoxamine; Lipocalin-2; Traumatic brain injury.