Mechanisms underlying the promotion of functional recovery by deferoxamine after spinal cord injury in rats
Jian Hao
Bo Li
Hui-quan Duan
Chen-xi Zhao
Yan Zhang
Chao Sun
Bin Pan
Chang Liu
Xiao-hong Kong
Xue Yao
Shi-qing Feng
摘要：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-1βand 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 ex-pression levels after spinal cord injury and inhibits apoptosis and glial scar formation to promote motor function recovery.
机标关键词：spinal cord injurymotor functionproinflammatory cytokinesprotein expressionfunction recoveryiron ionacidic proteiniron overload
资助基金：This study was supported by the National Natural Science Foundation of China, (No. 81672171, 81330042)the International Coop-eration Program of National Natural Science Foundation of China, (No. 81620108018)a grant from the Ministry of Science and Technology of China, (No. 2014DFR31210)a grant from the Tianjin Science and Technology Committee of China, (No. 13RCGFSY19000, 14ZCZDSY00044)the Youth Foundation of Tianjin Medical University General Hospital of China, (No. ZYYFY2015008)
论文发表日期：2017-01-01
在线出版日期：2025-08-15（本平台首次上网日期，不代表文献的发表时间）
页数：10( 959-968 )
英文信息