摘要
A rat model of spinal cord injury was established using modified Allen＇s method and treated with the ferric iron-chelating agent, deferoxamine. Hematoxylin-eosin, Nissl and Perl＇s Prussian blue staining, at 7 14 days following spinal cord injury, showed that following deferoxamine treatment, glial cells proliferation increased significantly, nerve cell morphology was improved and hemosiderin was significantly reduced in the injury region. At 1 56 days following injury, Basso, Beattie, and Bresnahan Locomotor Rating Scale scores were increased, while latencies of somatosensory-evoked potentials and motor-evoked potentials were decreased. Results demonstrate that deferoxamine can promote neurological functional recovery after experimental spinal cord injury in rats.
A rat model of spinal cord injury was established using modified Allen＇s method and treated with the ferric iron-chelating agent, deferoxamine. Hematoxylin-eosin, Nissl and Perl＇s Prussian blue staining, at 7 14 days following spinal cord injury, showed that following deferoxamine treatment, glial cells proliferation increased significantly, nerve cell morphology was improved and hemosiderin was significantly reduced in the injury region. At 1 56 days following injury, Basso, Beattie, and Bresnahan Locomotor Rating Scale scores were increased, while latencies of somatosensory-evoked potentials and motor-evoked potentials were decreased. Results demonstrate that deferoxamine can promote neurological functional recovery after experimental spinal cord injury in rats.
