| Central nervous system's (CNS) injury such as spinal cord injury produced by many types of trauma may cause neuron's degeneration and necrosis. Because of the lack of suitable microenvironment, the injured neuron of CNS can not regenerate, repair themselves and ultimately lead to serious sequel such as quadriplegia. Spinal cord injury contributes the heaviest burden to social and families. The loss of neurological function consequent to spinal cord injury occurs due to primary and secondary injury. The primary injury is produced directly by mechanical trauma such as spinal cord contusion or laceration injury. The extent of subsequent damage depends on several biomechanical factors associated with flexion, rotation or extension. The secondary injury such as hemorrhage and edema of local spinal cord that follows primary injury may enlarge the extent of damages and deteriorate neurological function of spinal cord. Posttraumatic inflammation is one of the initial processes that occur after spinal cord injury. Recruitment of leukocytes,monocytes,macrophages from the blood compartment to the site of inflammation represents one of the characteristic elements of the inflammatory process. On the one hand, these cells play an important role in removal of the tissue debris and produce substances such as glycoproteins and growth factors that are favorable for neurite growth and regeneration. On the other hand, these activated cells release a wide variety of lytic enzymes as they migrate through the extracellular matrix, as well as reactive oxygen and nitrogen intermediates following phagocytosis of bacteria and tissue debris that could promote progressive tissue damage and ischemia. Now, the phase of the secondary injury and chronic injury is amenable to therapeutic modulation. Glucocorticoids have been often utilized to modulate the secondary injury and chronic injury after spinal cord injury because they have the abilities of anti-inflammation,anti-oxidation,scavenging of free radicals,stabilization of lysosomal membranes,suppression of vasogenic edema and enhancement of spinal cord blood flow. Among glucocorticoids such as cortisone,prednisone,prednisolone,methylprednisolone,dexamethasone, methylprednisolone therapy has become the standard care in management of acute spinal cord injury due to its unique characteristics. High-dose of methylprednisolone administered early shows improvement outcome of spinal cord in experimental and clinical studies through modulating posttraumatic inflammationandsecondary injury significantly. However, methylpredniso-lone itself can not generate new neurons. So methylprednisolone therapy alone has not been sufficient to promote significant recovery following spinal injury. In the middle of 1990's, in vitro and in vivo experiments have shown that cells exist in the adult brain that are self-propagating and capable of producing all of the major neuronal cell types. Progress studies confirm that these cells come from neural stem cells. Neural stem cells have now been discovered in the adult human CNS and appear to behave similarly to their rodent counterparts. They distribute mainly in the CNS regions such as hippocampus and subventricular zone. Neural stem cells are multipotential cells that have the capacity to self-renew and the ability to generate both neurons and glia. Neural stem cells can be isolated from different areas and propagated for long periods in culture without losing their multi-potentiality. When transplanted back into the CNS, these neural stem cells can migrate, differentiate and integrate with host tissue and then express neurological function. This result changed the traditional concept that neuron of CNS could not regenerate and renew itself after injury. Now, neural stem cells' transplantation repairing CNS injury such as spinal cord injury becomes a hot point of neuroscience. However, little is known about what kind of neuron or myelin will regenerate after transplantation of neural stem cells. Concomitantly, there still lack of detailed...
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