摘要
After spinal cord injury （SCI）, a cascade of events begins. At first, there is physical damage with disruption of the blood-brain barrier （BBB） and the integrity of the nervous tissue. The disruption of central ner- vous system （CNS） BBB alters the endothelial permeability, the protein and chemokines expression and the propensity to release in situ inflam- matory cytokines, overcoming anti-inflammatory signals, facilitating the attraction and entry of immune system cells into the injured spinal cord parenchyma （Gaudet et al., 2011）. As a result, there is a neuroin- flammatory response with changes in blood flow, edema, cell infiltra- tion, apoptosis and release of axonal growth inhibitory factors. Nerve function loss occurs when the nerve impulse propagation is interrupted and do not reach its target. This disorder encompasses neuron and glia apoptosis, accompanied by Wallerian degeneration of disconnected axons, and CNS cells exposure to a hostile microenvironment that hampers axon regeneration （Mautes et al., 2000; Harkey et al., 2003）.
After spinal cord injury （SCI）, a cascade of events begins. At first, there is physical damage with disruption of the blood-brain barrier （BBB） and the integrity of the nervous tissue. The disruption of central ner- vous system （CNS） BBB alters the endothelial permeability, the protein and chemokines expression and the propensity to release in situ inflam- matory cytokines, overcoming anti-inflammatory signals, facilitating the attraction and entry of immune system cells into the injured spinal cord parenchyma （Gaudet et al., 2011）. As a result, there is a neuroin- flammatory response with changes in blood flow, edema, cell infiltra- tion, apoptosis and release of axonal growth inhibitory factors. Nerve function loss occurs when the nerve impulse propagation is interrupted and do not reach its target. This disorder encompasses neuron and glia apoptosis, accompanied by Wallerian degeneration of disconnected axons, and CNS cells exposure to a hostile microenvironment that hampers axon regeneration （Mautes et al., 2000; Harkey et al., 2003）.
