大鼠坐骨神经切断后Src抑制的蛋白激酶C的底物的表达变化

目的 探讨大鼠坐骨神经切断后,Src抑制的蛋白激酶C的底物(SSeCKS)在神经中的表达变化及其意义.方法 制备成年SD大鼠坐骨神经切断模型.通过Western blotting和免疫组织化学方法检测坐骨神经切断后SSeCKS表达的时空变化.结果 Western blotting显示,大鼠坐骨神经切断后,近端SSeCKS的表达逐步升高,伤后2d达到高峰,之后逐渐下降.远端SSeCKS表达于12h达到高峰,之后呈下降趋势.免疫组织化学方法结果表明,SSeCKS在神经断端处高表达,成簇状聚集;在远离断端处表达明显降低,分布亦较为均一.免疫荧光双标记结果显示,SSeCKS与S100、NF200及GAP43有部分共定位.结论 大鼠坐骨神经切断后,可以引起SSeCKS的表达变化,其可能参与周围神经损伤后某些伤害性刺激信号分子的转导,并与损伤后神经的再生及功能修复有关.

THE CHANGE OF SSeCKS AFTER THE TRANSECTION OF RAT SCIATIC NERVE

Objective To investigate the change of SSeCKS in sciatic nerve after the transection of rat sciatic nerve and its significance. Methods The sciatic nerve transection model of Sprague-Dawley rat was made.We tested the change of SSeCKS by Western blotting and immunohistochemistry. Results It showed from Western blotting that after injury,SSeCKS in the proximal lesion site increased gradually and reached its peak at 2d,then it began to decrease,while in the distal lesion site,SSeCKS peaked at 12h and then declined.Immunohistochemistry showed SSeCKS mainly located in break site,in a cluster expression pattern,while in the uninjury region,the level of SSeCKS was significantly lower and the distribution was uniform.The result of double immunofluorescent staining showed that SSeCKS partly colocalized with S100,NF200 and GAP43.Conclusion The transection of rat sciatic nerve can cause the change of SSeCKS and it might be involved in transduction of some harm stimulate signal moleculars after the injury.It may be also related with the nerve regeneration and function repair.