Mechanisms underlying the promotion of functional recovery by deferoxamine after spinal cord injury in rats.
Neural Regen Res. 2017 Jun;12(6):959-968. doi: 10.4103/1673-5374.208591.
Hao J1, Li B1, Duan HQ1, Zhao CX1, Zhang Y1, Sun C1, Pan B1, Liu C2, Kong XH2, Yao X1,3, Feng SQ1,3.
Author information
Abstract
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 T10 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-α and interleukin-1β 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-α, interleukin-1β, and caspase-3 expression levels after spinal cord injury and inhibits apoptosis and glial scar formation to promote motor function recovery.
KEYWORDS:
anti-inflammatory; deferoxamine; glial scar; interleukin-1β; apoptosis; iron; lipid peroxidation; motor function; nerve regeneration; neural regeneration; proinflammatory; rats; spinal cord injury; tumor necrosis factor-α

PMID: 28761430 PMCID: PMC5514872 DOI: 10.4103/1673-5374.208591

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