大鼠坐骨神经损伤后Src抑制的蛋白激酶C的底物在背根神经节中的表达变化

Change of Src-suppressed C kinase substrate in dorsal root ganglion after injury of sciatic nerve in rat

目的:探讨大鼠坐骨神经损伤后,Src抑制的蛋白激酶C的底物(SSeCKS)在背根神经节(DRG)中的表达变化及其意义。方法:制备成年SD(Sprague-Dawley)大鼠坐骨神经夹伤及切断模型。通过Western印迹法、Real-time PCR及免疫组织化学方法检测坐骨神经损伤后SSeCKS在DRG中表达的时空变化。结果:大鼠坐骨神经夹伤后6h,DRG中可检测到SSeCKS的表达并逐步升高,伤后12h达到高峰,2d后逐渐下降;而大鼠坐骨神经切断后DRG中SSeCKS的表达高峰发生在伤后2周,1d时最低;SSeCKS主要分布于DRG大、中、小神经元胞质;SSeCKS与NeuN、NF200以及GAP43存在共定位。结论:大鼠坐骨神经损伤后,引起DRG中SSeCKS的表达变化,其可能参与疼痛信号转导通路并与周围神经损伤后的再生有关。

Objective： To investigate the change of Src-suppressed C kinase substrate （SSeCKS） in dorsal root ganglion （DRG） after injury of sciatic nerve in rats. Methods： Sciatic nerve crush model and transection model of SD rats were established. The change of SSeCKS was detected by Western blotting, Real-time PCR and immunohistochemistry. Results： Six hours after crush injury, SSeCKS could be found in DRG and increased gradually, and reached its peak at 12 h. Two days later, it began to decrease. While after sciatic nerve transection, SSeCKS reached its peak at 2 w and the lowest expression was found at 1 d; SSeCKS was mainly located in cytoplasm of the large, middle and small neurons of DRG and it was colocalized with NeuN, NF200 and GAP43. Conclusion： The injury of rat sciatic nerve can cause the change of SSeCKS in DRG and it may be involved in signal transduction of pain access and the regeneration of peripheral nerve.