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Preliminary Inquiry of Injury and Repair Facts in Rats Spinal Cord after Chronic Compress

Author: ZhouChangZuo
Tutor: AnChunHou
School: China Medical University
Course: Surgery
Keywords: Chronic compression Spinal cord injury Apoptosis Animal models BBB score Nestin
CLC: R651.2
Type: Master's thesis
Year: 2009
Downloads: 52
Quote: 0
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Abstract


The purpose of the experiment to establish a new spinal cord of rats with chronic constriction injury model, lay the foundation for exploring the pathophysiological mechanisms of spinal cord compression. Explore apoptosis in chronic compression injury law, detect nestin (neural stem cell marker protein) expression pattern in the spinal cord of rats after chronic injury. The experimental method in this experiment to improve the previous chronic the expansion materials oppression model materials surgically implanted oppression, avoid direct damage in the implantation process. Under the microscope, the of rat thoracic 7,8 bilateral pedicle cut, remove the lamina, implanted an absorbent slowly expanding material, along with the expansion of oppression was gradually formed varying degrees of chronic spinal cord compression injury in experimental animals model. 40 wista rats were randomly divided into operation group 30, control group 10. The control group of the same surgery, but not implanted oppression was. Were observed after the rats had symptoms of paralysis of the lower limbs, considered to be due to intraoperative injury to put to death, are not included in the statistics. Postoperative penicillin anti-inflammatory therapy five days. 1,3,7,14,28 days after surgery BBB score functional evaluation of the behavior detection oppression spinal cord pathology specimens and semi-quantitative detection of apoptosis by computerized image analysis system to start gene P53 and application TUNEL-staining apoptosis . Immunohistochemical detection of nestin (nestin). The experimental results were observed after the behavior, histology, pathological changes, consistent with all three. Chronic compressed spinal cord model was established. The apoptotic cells were mainly distributed in the white matter longitudinal conduction of the beam on the area of ??demyelination, mainly oligodendrocytes. Expression of apoptosis first day, the third day of the expression reached a peak, continued until the seventh day, and then decreased. P53 situ hybridization showed that one day after surgery, nerve cells, glial cells appeared positive expression increased the most obvious expression of the first three days, to of 7 Telsda to a peak, after steady at a relatively stable level . Chronic injury, nestin expression in the ependymal and around. Injury after the first day of nestin expression one week after injury, reached a peak two weeks began to rise again, 28 days almost no expression. The experimental results compared to the previous model, this model has the advantages of producing simple to adjust the degree of injury, spinal cord injury can exhibit different degrees of oppression, and repeatability. Laid the foundation for further study of the pathological mechanisms of chronic spinal cord compression injury. Chronic compressive spinal cord injury can lead to a large number of apoptosis, while activation of endogenous protective mechanism, the spinal cord becomes adaptive change. Apoptosis in glial cells from the earliest to the changes caused by changes in nerve cells of the micro-environment in the Spinal Cord. Start early apoptotic genes in rat spinal cord pathophysiological changes and behavioral changes of decompression provides a theoretical basis for early clinical. Injury, if we can activate and regulation of the expression of the neural stem cells, will greatly improve the efficiency of the self-repair of spinal cord injury.

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CLC: > Medicine, health > Surgery > Of surgery > Head and Neurosurgery > Spinal cord
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