NFB signal pathway and secondary injury in acute spinal cord injury research progress.doc

 PAGE \* MERGEFORMAT 16 NFB signal pathway and secondary injury in acute spinal cord injury research progress [Abstract] spinal cord injury is a serious threat to human health, the common trauma, primary and secondary points. Secondary injury after spinal cord injury patients are often the main damage. In recent years, nuclear transcription factor found (NF B signaling pathway inflammatory cells in the spinal cord injury, neurons and endothelial cells activation, mainly through the activation of the NF B regulate transcription of target genes resulting products (such as cytokines, adhesion molecules and inducible nitric oxide synthase, etc. to participate in secondary damage process. This article NF B signaling pathway in acute spinal cord injury secondary to trauma are reviewed. [Keywords:] nuclear factor B, spinal cord injury Abstract: Spinal cord injury is a kind of common injury that seriously threatens human health.The secondary injury caused by spinal cord injury is always the main damage for patients in later stage.It is found that NF B signal pathway is also activated in inflammatory cells , neurons and endothelial cells after spinal cord injury.Activated NF B signal pathway takes part in the course of secondary injury by regulating products resulting in target gene transcription (for instance: cytokines, adhesion molecules, inducible nitric oxide synthase, etc .. NF B signal pathway and the acute secondary injury in spinal cord injury are discussed in this paper. Keywords:: NF B, spinal cord injury Spinal cord injury is a serious threat to human health, a common injury, often caused by physical sensation, motor function and autonomic dysfunction. Spinal cord injury, including primary and secondary injury, primary injury is often hit with the primary mechanical intensity and scope related to secondary injury after spinal cord injury in a variety of factors of primary spinal cord caused by injury, spinal cord injury produced by primary inj