| ObjectiveEstablishment of a new spinal cord in rats with chronic constriction injury model of spinal cord compression to explore the physiological mechanism of the pathological basis. Explore the chronic constriction injury of nestin (nestin neural stem cell marker protein) expression and significance of law.MethodOur predecessors in this experiment improved model of the chronic expansion of material oppression, by way of surgical implant materials, oppression, avoiding direct injury during implantation. At under a microscope, the rat thoracic 7,8 bilateral pedicle cut off, remove the lamina, embedded in a water-swelling material, with the oppression of the expansion of material, and gradually developed different degrees of chronic compressive spinal cord injury in experimental animal models.40 wistar rats were randomly divided into operated group 30, control group 10. The control group in which to perform the same surgery, but does not implant material oppression. After observation, such as the rat appeared both lower extremities paralysis symptoms, considering the damage caused by surgery, death, not included in the statistics. Penicillin anti-inflammatory treatment after 5 days.1,3,7,14,28 In the first days after surgery through the BBB score for behavioral function evaluation, taken from 5mm from the edge of spinal cord compression, sham-operated rats as control group, pathological examination and nestin-line immune staining, semi-quantitative reverse transcription-polymerase chain reaction (reverse transcription-polymerase chain reaction, RT-PCR) determination of the expression of nestin mRNA, the computer image analysis system quantitative analysis, simultaneous measurement of pressure relief section of the spinal canal diameter and thickness swelling material occupation. Thickness of canal encroachment rate=occupied/oppressed section of canal diameter. ResultsIn this study, the establishment of rat chronic compressive spinal cord injury model behavior after the observation, histology and pathology testing, three in line. Chronic compression of spinal cord injury model was established. Nestin-positive processes extended to the gray tree, in the gray matter of the expression was mainly distributed in the vicinity of neurons and blood vessels around the injury began the first day of expression 1 week after injury, reached a peak two weeks began to decline,4 weeks, almost no expression. Model building has been detected 24 hours after the nestin mRNA,1 week and up to the peak, then gradually decreased.ConclusionThis model model than in the past to compare with the production of simple, adjustable degree of injury, spinal cord injury can show different levels of oppression, repeatability strong advantages. To further study the pathogenesis of spinal cord compression injury in chronic basis. Pathology results showed that injury at 3-7 days after compression spinal cord tissue liquefaction necrosis, scarring, and the gradual emergence of a reduced number of nerve cells and neural glial cell proliferation, while the BBB score and pathological changes in rat spinal cord in 7 days after the change in rapidly, suggesting that early decompression! Nestin for neural stem cells, precursor cells of the marker proteins, protein expression after spinal cord injury-positive cells in the repair of spinal cord itself may play an active role. With chronic spinal cord injury can cause nest nestin protein and mRNA in the spinal cord white matter, gray matter and central canal ependymal cells, and show some variation, there is expression after injury, peaked at 1 week,2 weeks began to decline, Thus, spinal cord injury time to take the appropriate line of neural stem cell transplantation, there may be conducive to injury repair and functional reconstruction. In addition, after injury and regulation if they can activate the expression of neural stem cells, which may greatly enhance the efficiency of self-repair spinal cord injury. |
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