| BackgroundPrimary injury and secondary injury mechanisms are involved in the development and progress of pathology after acute spinal cord injury (SCI). Primary injury occurrs shortly after mechanical insult and causes neurological dysfunction which is irreversible. Secondary injury is a complex self-destruction cascade reaction procedure which is a major cause in further reduction of functional recovery, but the exact mechanisms of secondary injury are still not well understood. Previous studies have demonstrated that SCI-induced inflammatory responses play an important role in the secondary injury, and the early inflammatory responses can trigger a series of reaction on the level of cell and molecular of injured spinal cord, resulting in the development of scar tissue, as well as necrosis or apoptosis of neuron and oligodendrocyte, which may lead to a further deterioration of functional outcome. By attenuating SCI-induced inflammatory responses directly or indirectly, the neurological dysfunction will be alleviated. So far, the convincible mechanism involved in the development and progress of the inflammatory responses after SCI is not quite clear. Cytokines and chemokines are an important component of the chain of the inflammatory responses, which participate and regulate the process concerned. Cytokines are divided into proinflammatory and anti-inflammatory cytokines according to the regulation of inflammatory responses. Chemokines are subdivided into CC, CXC, CX3C and C four groups which associated with recruitment of inflammatory cells. Numerous studies have demonstrated proinflammatory cytokinesand chemokines are significantly up-regulated following brain injury, and it aggravate brain post-injury inflammatory responses and play an important role in the pathologic development of secondary brain injury. It has been reported that proinflammatory cytokines and chemokines were also up-regulated significantly at the lesion site after SCI, which augmented the inflammation cascade reaction and aggravated the injury of the spinal cord. According to this, a further study of the changes of the cytokines and chemokines after SCI will do good to the modulation of the inflammation of SCI and provide some ideas to develop new anti-inflammatory strategies for SCI.Erythropoietin (EPO), 34kd, is a sialoglycoprotein. EPO was considered to be excreted only by the kidney and responsible for the proliferation, maturation, and differentiation of the precursors of the erythroid cell line incretory hormone. Recent studies have demonstrated that, in addition to kidney, liver, lung, spleen, placenta and procreative organ can excrete EPO. EPO and its receptors (EPOR) are widely expressed in the central nervous system(CNS). EPO, a multifunctional nutritional factor and neuroprotective factor, which can modulate the inflammatory and immune response, not only plays a crucial role in the regulation of erythropoiesis, but also plays a crucial role in the regulation neurodevelopment, and have neuroprotective function in different conditions of neuronal damage. The exact mechanism of EPO neuroprotective effect after the injury of CNS are still not well understood. One of the possible mechanism is anti-inflammation role of EPO. In experimental rat models of brain injury. EPO counteracts post-traumatic inflammatory responses and have the neuroprotective function. In rat models of experimental autoimmune encephalomyelitis and infarction of median artery of cerebrum, EPO reduces cytokines and chemokines production attenuates inflammatory responses. However, the effect of EPO on cytokines and chemokines production after contusion injury of the cord spine, as well as the neuroprotective role, is not clear. ObjectiveTo study the expressions of cytokines and chemokines in the rat spinal cord after SCI; To investigate the effect of recombinant human erythropoietin (rHuEPO) on cytokines and chemokines in the rat spinal cord after SCI and its effectiveness inpromoting neurologic recovery after an incomplete rat SCI. MethodsIn the presen... |
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