脊髓型减压病大鼠脊髓组织内NGF和Trk A的蛋白表达

目的 观察大鼠脊髓减压病后脊髓组织内神经生长因子（NGF）及其受体酪氨酸激酶A（Trk A）蛋白表达随疾病进程的变化过程，探讨减压病脊髓损伤后自身的神经保护机制。方法 采用1.0MPa暴露5.5min后极快速减压的方法制备SD大鼠脊髓减压病模型，在出舱0，6，24，48，72h应用免疫组织化学染色和半定量图象分析方法检测脊髓组织NGF及其受体Trk A的蛋白表达。结果 极快速减压后6h开始有少量NGF和Trk A蛋白表达，在24h表达明显增强并达到高峰，此后Trk A表达逐渐减弱，NGF表达直到72h仍比基础值明显增加。结论减压病脊髓损伤诱导了脊髓神经元和胶质细胞的NGF及其受体的合成，提示脊髓型减压病在损伤神经组织的同时也激活了自身的神经保护机制，通过Trk A受体途径NGF可能在保护受损神经细胞中起作用。

Time course of protein expression of NGF and Trk A in the spinal cord of rats suffering from spinal cord decompression sickness

Objective To study the time course change of nerve growth factor (NGF) and its receptor tyrosine kinase A (Trk A) in a rat model of spinal cord decompression sickness, and explore to the auto nerve protective mechanism. Methods SD Rats, masculine, were randomly divided into control group, safety decompression group, spinal cord decompression sickness group. A rat model of spinal cord decompression sickness was set up by exposing rats to 1.0 MPa for 5.5 min and then decompressing in 55 s. The expression of NGF and Trk A were detected by immunohistochemistry at 0,6,24,48 and 72 h. Results There was a small quantity of positive stain of NGF and Trk A at 6 h,which increased obviously and came to peak at 24 h. Then, the expression of Trk A decreased in 48 h,while NGF was increased until 72 h. Conclusions Decompression sickness induced nerve damage, and simultaneously initiated factors of spinal cord auto-protection mechanism.