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The purpose of the secondary mechanism of spinal cord injury and its treatment research more and more attention by everyone. Hypoxia-inducible factor-1α is an important discovery in the 1990s, the oxygen sensor - signal transduction - the effects of gene hypoxia response pathway. Most scholars believe that HIF-1α is induced by hypoxia gene and maintain a stable environment within the cell oxygen core factor, can regulate energy metabolism, angiogenesis, apoptosis, cell differentiation, matrix synthesis and gene expression. The experimental rat secondary spinal cord injury by observing hypoxia-inducible factor-1α (HIF-1α) expression of the law, to investigate its role in the development process in secondary spinal cord injury occurs. Methods 66 SD rats were randomly divided into a control group the fake injury group and the experimental group h (injury, 3h, 6h, 12h, 1d, 2d, 3d, 7d, 14d). The experimental group to establish hydrostatic spinal cord injury model in rats injured rat T 10 spinal cord, sham group only laminectomy. Rats in each group to the corresponding point in time were killed, and 40 g / L paraformaldehyde perfusion fixed take damage spinal cord is approximately 10.0mm HE staining and immunohistochemical staining. Different times after the detection of secondary spinal cord injury, spinal cord tissue pathological changes and injury HIF-1α expression timing. Results found: brown particles appeared positive in the cytoplasm or nucleus. Each slice optional 10 vision, to count the number of positive cells. The data used SPSSV11 package handling. Results visible local tissue congestion of the spinal cord injury in rats. Microscope after SCI 3 ~ 6h damage local neurons nuclear pyknosis, cell body narrow, deep-eosin staining cytoplasm. After injury, 1 ~ 3d, axon swelling, vacuoles, the quality within nerve myelin scattered, the disintegration broken. 3 ~ 7d gliosis after injury, the visible satellite phenomenon and ghosting cells. After injury, 14d, part of the gray matter of spinal cord injury thinning disintegration necrosis, showing the formation of cysts. Rarely detected in normal spinal cord tissue cells HIF-1α, sham group slightly increased, but not statistically significant (P> 0.05). Hours after injury, HIF-1α positive products began to increase, mainly in the spinal anterior horn neurons and a small amount of glial cells in the expression; 1 day after injury, reached the peak positive products can be found in the spinal cord neurons, glial cells, ependymal cells and vascular endothelial cells within the stromal its subcellular localization in cytoplasm and nucleus. HIF-1α immunoreactive cells in 1 ~ 3h period after injury has been maintained at a high level, then gradually decreased to 14d after injury, only seen in a small amount of white matter in the glial cells. The significant difference between the experimental group (P <0.05). Conclusion HIF-1α expression after spinal cord injury began to increase, and by the precise control of the partial pressure of oxygen in the cells, the protein expression of HIF-1α and secondary spinal cord injury is closely related to ischemia and hypoxia, its expression pattern and correlation of injury time . HIF-1α may be involved in the protection and restoration of the neurons.
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