大鼠急性脊髓损伤后Caspase-3、Cathepsin B的表达

Expression and significance of cathepsin B after acute spinal cord injury

[目的]研究大鼠急性脊髓损伤后Caspase-3、Cathepsin B的表达,并初步探讨Caspase-3、Cathepsin B在脊髓损伤后表达的意义。[方法]将78只成年健康SD大鼠按Nystrom法建立大鼠脊髓(T8、T9)急性压迫损伤模型,HE染色观察脊髓组织病理学变化,免疫组化测定各时间点Cathepsin B、Caspase-3的表达变化,原位末端脱氧核糖核酸转移酶介导的脱氧尿苷三磷酸(dUTP)标记法(TUNEL法)检测神经细胞的凋亡水平。[结果]免疫组化结果显示正常及假手术组大鼠脊髓神经细胞中Caspase-3,Cathepsin B,TUNEL阳性细胞较少;在脊髓损伤后3dCathepsin B阳性细胞数明显增多,5d达高峰,7d未见明显衰减。Caspase-3阳性细胞数在脊髓损伤后8h明显增多,3d达高峰,7d表达减弱。TUNEL阳性细胞数也在8h明显增多,3d达高峰,7d表达减弱。Cathepsin B阳性细胞形态及表达的部位均与Caspase-3阳性细胞、TUNEL阳性细胞差别较大。[结论]Caspase-3参与了脊髓损伤细胞凋亡的调节,

[ Objective ] To study the expression of Cathepsin B, Caspase-3 and to explore the significance of their expression initially after acute spinal cord injury in rats. [ Method ] The spinal cord injury of the healthy adult SD rats （ 78 ） was induced with Nystrom＇ s way by the moderate compression at the level of T8 and T9 spinal cord. HE methods were used to detect the path- ologic change of spinal cord. The expression of Cathepsin B and Caspase-3 were detected by immunohistochemical study. Be- sides ,using the terminal deoxynucleotidyl transferase mediated DUTP nick and labeling （TUNEL） methods to detect the level of the apoptosis of neural cells. [ Result] There were few expressions of Cathepsin B, Caspase-3 and TUNEL positive cells in normal and sham operated spinal cord as detected by immunohistochemical study. The number of positive cells of Cathepsin B increased clearly at 3 days, reached a peak at 5 days, and was constant at 7 days after injury. While the expression of Caspase-3 increased obviously at 8 hours,got to a peak at 3 days,and was lowest at 7 days. And the number of positive cells of TUNEL also increased obviously at 8 hours, got to a peak at 3 days, and was lowest at 7 days. There were significance differences of morphological and position of positive cells between Cathepsin B and Caspase-3 or Tunel. [ Conclusion] Caspase-3 protein expressions are enhanced in combination with neuronal apoptosis, while Cathepsin B may involve in the secondary injury by inflammatory cells after acute spinal cord injury.