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Spinal cord injury (spinal cord injury SCI) severely affected by the human body, especially in the young population of high incidence, most spinal cord injuries are caused by the accident, human physical and psychological as well as family and social tremendous burden. Therefore, the mechanism of disease after spinal cord injury research scholars from various countries as the current focus of the study. Including primary injury and spinal cord injury secondary injury, primary spinal cord injury is initially subjected to mechanical damage arising from partial destruction of nerve tissue; secondary injury occurs in the primary injury, mainly as damage zone continues to expand, and a series of pathological changes. As rich in blood vessels in the spinal cord, so after spinal cord injury in the blood vessels have also been destroyed, affecting blood spinal cord barrier function. Microglial cells in the nervous system exist as immune cells after spinal cord injury also occurred activation, migration, phagocytosis of necrotic tissue to the damaged area and generate inflammatory cytokines, and spinal cord injury are closely related. After spinal cord injury in the study on the mechanism of people have done a lot of research, but at present the blood spinal cord barrier after spinal cord injury and changes in the activation of microglia relationship between the two is unclear. To this end we crush injury in rats as a model to study the blood spinal cord barrier after spinal cord injury and microglia in the relationship between changes. We use spinal cord crush injury model, the choice of different time points after injury, spinal cord injury was observed after activation of microglia BSCB function status. In the experiment, we used HE staining pathological changes after spinal cord injury, measured after SCI 0h, 8h, 24h, 72h, 1w, 2w, 4w damaged area when, at each time point were 0.47 ± 0.11mm2, 1.60 ± 0.60mm2, 1.80 ± 0.57mm2, 3.88 ± 1.86mm2, 3.51 ± 1.29mm2, 2.33 ± 0.53mm2, 2.23 ± 1.44mm2. We use specific markers of microglia OX-42 was observed by immunofluorescence staining microglia, femoral vein injection of Evans blue was observed changes in blood spinal cord barrier. The results showed that: in 24h after injury group observed activated microglia and subsequently migrate into the damaged part of the region, phagocytosis of necrotic tissue, the formation of macrophages. Activated microglia can exist for a long period of time. And when the spinal cord is no longer 1w Evans blue blood spinal cord barrier back to normal. Microglia activation and blood spinal cord barrier, said the closure is in inconsistent instructions to activate microglia enough to destroy the blood spinal cord barrier. In conclusion, spinal cord injury activation of microglia and blood spinal barrier closure inconsistency in time, the activation of microglia not affect the closure of the blood spinal barrier. Secondary injury at 72h, the maximum damage area to the formation of hollow when 2w, damage zone stabilized.
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