Observation of cell apoptosis and BDNF expression in spinal cord injured by chronic compression

LI Xiao-dong; XU Jun

doi:10.13798/j.issn.1009-153X.2016.03.012

Abstract：Objective To explore the pathogenetic mechanism of injury to spinal cord caused by chronic compression. Methods Seventy-five SD rats were divided into three groups of 25 animal each, i.e. normal group, experimental group, in which the model of spinal cord injury was caused by the chronic compression and control group which was similar to the experimental group in surgical treatment except the chronic compression of the spinal cord. The spinal cord function was determined by Basso, Beattie and Bresnahan locomotor rating scale (BBB Scale) postoperatively 1, 7, 14, 21 and 28 days after the pressure issues in all the groups, in which cells apoptosis and the expression of brain derived neurotrophic factor (BDNF) and its receptor, tropomyosin receptor kinase B (Trk B) in the injured spinal cord were determined respectively by TdT-mediated duTP nick-end labeling (TUNEL) and immunohistochemical staining 28 days after the pressure issues. Results BBB scores were significantly lower in the experimental group than those in the other two groups 1, 7, 14, 21 and 28 days after the pressure issues (P<0.05). TUNEL staining showed that there were apoptosis of many cells in the injured spinal cord tissues in the experimental group and no cells apoptosis was found in the other two groups. The immunohistochemical staining showed that the expressions of BDNF and its receptor TrkB were stronger in the spinal cord tissues in the experimental group than those in the other two groups. Conclusion Apoptosis and the expression of BDNF, TrkB in the spinal cord injured by chronic compression, which can cause significant injury to the spinal cord function, are significantly enhanced.