Journal
NEURAL REGENERATION RESEARCH
Volume 12, Issue 6, Pages 959-968Publisher
WOLTERS KLUWER MEDKNOW PUBLICATIONS
DOI: 10.4103/1673-5374.208591
Keywords
nerve regeneration; spinal cord injury; deferoxamine; tumor necrosis factor-alpha; interleukin-1 beta; apoptosis; iron; anti-inflammatory; glial scar; proinflammatory; rats; motor function; lipid peroxidation; neural regeneration
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Funding
- National Natural Science Foundation of China [81672171, 81330042]
- International Cooperation Program of National Natural Science Foundation of China [81620108018]
- Ministry of Science and Technology of China [2014DFR31210]
- Tianjin Science and Technology Committee of China [13RCGFSY19000, 14ZCZDSY00044]
- Youth Foundation of Tianjin Medical University General Hospital of China [ZYYFY2015008]
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Deferoxamine, a clinically safe drug used for treating iron overload, also repairs spinal cord injury although the mechanism for this action remains unknown. Here, we determined whether deferoxamine was therapeutic in a rat model of spinal cord injury and explored potential mechanisms for this effect. Spinal cord injury was induced by impacting the spinal cord at the thoracic T-10 vertebra level. One group of injured rats received deferoxamine, a second injured group received saline, and a third group was sham operated. Both 2 days and 2 weeks after spinal cord injury, total iron ion levels and protein expression levels of the proinflammatory cytokines tumor necrosis factor-alpha and interleukin-l beta and the pro-apoptotic protein caspase-3 in the spinal cords of the injured deferoxamine-treated rats were significantly lower than those in the injured saline-treated group. The percentage of the area positive for glial fibrillary acidic protein immunoreactivity and the number of terminal deoxynucleotidyl transferase dUTP nick end labeling-positive cells were also significantly decreased both 2 days and 2 weeks post injury, while the number of NeuN-positive cells and the percentage of the area positive for the oligodendrocyte marker CNPase were increased in the injured deferoxamine-treated rats. At 14-56 days post injury, hind limb motor function in the deferoxamine-treated rats was superior to that in the saline-treated rats. These results suggest that deferoxamine decreases total iron ion, tumor necrosis factor-alpha, interleukin-1 beta, and caspase-3 expression levels after spinal cord injury and inhibits apoptosis and glial scar formation to promote motor function recovery.
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