中文摘要：

目的：探讨大鼠坐骨神经损伤早期NF—KB和Bcl-2在脊髓中的表达变化。方法：健康成年sD大鼠48只，随机分为正常组、假手术组和右侧坐骨神经压榨组，动物存活不同时问（6，12，24和72h）获取L。脊髓段，用免疫组织化学方法检测脊髓内NF—KB和Bcl-2的表达变化。结果：（1）正常L4-6脊髓内，NF—KB和Bcl-2免疫阳性产物主要位于前角运动神经元胞浆内，NF—KB活化少，Bcl-2表达低；（2）损伤后双侧脊髓中NF—κB免疫阳性产物则主要位于胞核内，呈活化状态，损伤侧活化起始时问（6h）早于损伤对照侧（12h），且6、12、24hNF—κB活化细胞数明显高于对照侧（P〈0．05），72h双侧比较无明显差异（P〉0．05）。（3）损伤后6h损伤侧脊髓中Bcl-2免疫阳性反应即增强，12h达到高峰，24h下降，72h又增高；其中6、12、72h损伤侧Bcl-2免疫阳性反应灰度值与对照侧和正常组相比差别具有统计学意义（P〈0．05），而24h损伤侧与对照侧和正常组比较无统计学差异（P〉0．05）。结论：坐骨神经损伤后脊髓前角细胞中NF—κB的活化，激活了其下游抗凋亡基因Bcl-2的转录，两者可能在损伤早期参与抑制细胞凋亡，促进细胞存活和神经再生。

英文摘要：

Objective： To investigate the expression profiles of NF-κB and Bcl-2 in rats spinal cord after sciatic nerve injury. Methods： Total 48 adult Sprague-Dawley rats were randomly divided into normal control, sham-operation and sciatic nerve crush group, the later was further divided into four subgroups according to different survival time （6,12,24,72 hours） respectively. The expression of NF-κB and Bcl-2 in L4-6 spinal cord was detected by immunohistochemistry. Results： （1） In normal and sham-operated rats, the immuno-positive products of NF-κB and Bcl-2 were found mainly in spinal motor neuron cytoplasm; there were few nuclear stained NF-κB activated cells and low expression of Bcl-2. （2） After sciatic nerve injury, nuclear positive NF-κB activated cell number significantly increased in experimental groups fi, om hour 6 in ipsilateral side and from hour 12 in contraleteral side, and both peaked at hour 24, but declined to normal level at 72h, as compared to the control groups. （3） 6h after injury, Bcl-2 expression was significantly up-regulated in ipsilateral spinal motor neurons, peaked at hour 12, and declined at hour 24, but turned to increase at hour 72. Conclusion： Our data demonstrate that crush injury of rat sciatic nerve induce the activation of NF-κB and a subsequent increase of Bcl-2 expression in spinal motor neurons. These data suggest that these two proteins may participate in the process of anti-apoptosis and promoting cell survival and neuronal regeneration after nerve injury.