Chapter title |
Deferoxamine Attenuated the Upregulation of Lipocalin-2 Induced by Traumatic Brain Injury in Rats
|
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Chapter number | 50 |
Book title |
Brain Edema XVI
|
Published in |
Acta neurochirurgica Supplement, January 2016
|
DOI | 10.1007/978-3-319-18497-5_50 |
Pubmed ID | |
Book ISBNs |
978-3-31-918496-8, 978-3-31-918497-5
|
Authors |
Jinbing Zhao, Guohua Xi, Gang Wu, Richard F. Keep, Ya Hua |
Abstract |
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. |
Mendeley readers
Geographical breakdown
Country | Count | As % |
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Unknown | 10 | 100% |
Demographic breakdown
Readers by professional status | Count | As % |
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Student > Doctoral Student | 2 | 20% |
Student > Master | 2 | 20% |
Student > Bachelor | 2 | 20% |
Other | 1 | 10% |
Researcher | 1 | 10% |
Other | 1 | 10% |
Unknown | 1 | 10% |
Readers by discipline | Count | As % |
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Medicine and Dentistry | 3 | 30% |
Agricultural and Biological Sciences | 2 | 20% |
Biochemistry, Genetics and Molecular Biology | 2 | 20% |
Physics and Astronomy | 1 | 10% |
Neuroscience | 1 | 10% |
Other | 0 | 0% |
Unknown | 1 | 10% |