Deferoxamine Attenuates Acute Hydrocephalus After Traumatic Brain Injury in Rats
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Acute post-traumatic ventricular dilation and hydrocephalus are relatively frequent consequences of traumatic brain injury (TBI). Several recent studies have indicated that high iron levels in brain may relate to hydrocephalus development after intracranial hemorrhage. However, the role of iron in the development of post-traumatic hydrocephalus is still unclear. This study was to determine whether or not iron has a role in hydrocephalus development after TBI. TBI was induced by lateral fluid-percussion in male Sprague–Dawley rats. Some rats had intraventricular injection of iron. Acute hydrocephalus was measured by magnetic resonance T2-weighted imaging and brain hemorrhage was determined by T2* gradient–echo sequence imaging and brain hemoglobin levels. The effect of deferoxamine on TBI-induced hydrocephalus was examined. TBI resulted in acute hydrocephalus at 24 h (lateral ventricle volume: 24.1 ± 3.0 vs. 9.9 ± 0.2 mm3 in sham group). Intraventricular injection of iron also caused hydrocephalus (25.7 ± 3.4 vs. 9.0 ± 0.6 mm3 in saline group). Deferoxamine treatment attenuated TBI-induced hydrocephalus and heme oxygenase-1 upregulation. In conclusion, iron may contribute to acute hydrocephalus after TBI.
KeywordsDeferoxamine Hydrocephalus Lateral fluid percussion Traumatic brain injury
This study was supported by grants NS-073595, NS-079157 and NS-084049 from the National Institutes of Health (NIH) and grants 81301049 and 30872675 from NSFC. The content is solely the responsibility of the authors and does not necessarily represent the official views of the NIH and NSFC.
Conflict of Interest
Jinbing Zhao, Zhi Chen, Guohua Xi, Richard F. Keep and Ya Hua declare that they have no conflict of interest.
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