Expression of apoptosis-related protein in motor neurons of anterior horn of the spinal cord after acute cauda equina compression / 中国组织工程研究

ABSTRACT

BACKGROUND:Cauda equina syndrome often induces skin hypoesthesia in the perineal area, poor urine-stool control, and impairs male function. After peripheral nerve fiber injury, apoptosis of neurons appeared. This is associated with the nature of the injury, the types of neurons, the species of animals, the age, and the distance between neurons. OBJECTIVE:To explore the motor neuron apoptosis and expression of apoptosis-associated protein in the anterior horn of the spinal cord after acute cauda equina compression. METHODS:A total of 27 canines were randomly divided into three groups. In the compression and control groups, models of cauda equina compression were established. In the normal group, no models were established. Compression group received water sac compression for 4, 8, 12, 24, 48, 72 and 168 hours, with three models in each group. In the control group, only water sac was implanted, but water was not injected. Terminal deoxynucleotidyl transferase TdT-mediated biotin dUTP nick end-labeling assay was used to detect the apoptosis of neurons in the anterior horn of the spinal cord. Bcl-2, Bax and Caspase-3 protein expressions were measured by immunohistochemical staining (strept avidin-biotin complex). Gray values of positive cels of Bax, Bcl-2 and Caspase-3 protein expressions were detected using Qwin550Cw image colection and analysis system. RESULTS AND CONCLUSION:The apoptosis of motor neuron occurred in the compression groups. At 12 hours of compression, positive cels were detected, and the number of positive cels reached a peak at 72 hours. Bax and Bcl-2 protein expression was smal in the normal group. Caspase-3 protein expression was not detected in the normal and control groups. Bax and Bcl-2 protein expression was significantly increased at 8 hours, peaked at 72 hours and reduced to a normal level at 168 hours. The increased range of Bax protein expression was bigger than that of Bcl-2. Caspase-3 protein began to express at 12 hours, peaked at 72 hours and reduced to a low level at 168 hours. Bax and Caspase-3 protein expression peaked at 72 hours, and Bcl-2 protein expression was not obviously increased. These findings verified that after acute cauda equina compression, the apoptosis of neurons occurred in the anterior horn of the spinal cord. Bax and Bcl-2 protein expression showed an antagonistic action. In the Bax/Bcl-2 complex, Bax protein in a high expression promoted apoptosis, induced Caspase-3 protein expression, and neuronal apoptosis.