APOPTOSIS AND ULTRASTRUCTURAL CHARACTERISTICS AFTER SPINAL CORD INJURY IN RATS

Shuai Peng, Xiangyang Liu, Lei Chang, Bin Liu, Mingyan Zhang, Xiongjie Shen^*

Department of Spine Surgery, Hunan Provincial People's Hospital, Changsha, 410005, China

Background: Spinal cord injury (SCI) is severe trauma to the central nervous system with complete or incomplete loss of sensory, motor, and sphincter function below the injury level. Secondary cell death after spinal cord injury is not directly due to injury but due to cell apoptosis. How to inhibit cell apoptosis is the key to protecting neurons and repairing spinal cord injury. It is also important to observe the ultrastructure after spinal cord injury in rats, and the work of various organelles in cells after spinal cord injury. This paper aims to study the apoptosis and ultrastructural characteristics after spinal cord injury in rats. 

Method: In this paper, rats are used as experimental subjects to study the apoptosis and ultrastructural characteristics after spinal cord injury in rats, and combine the expression of autophagy-related proteins Beclin1, LC3B and the relationship between their expression and injury time after spinal cord injury. 

Result: It will explain the expression and role of autophagy after spinal cord injury. It will also explain the spinal cord injury from another level by studying the expression of autophagy in various nerve cells in the spinal cord and the possible connection between autophagy and apoptosis, after the cell response, and preliminary evaluation of the role of autophagy in spinal cord injury. 

Conclusion: The results showed that the expression of SIRT1 and the downstream protein foxo4 increased after spinal cord injury, suggesting that deacetylation of the SIRT1 signaling pathway in the subacute phase may have a neuroprotective effect. The expression of β-catenin is up-regulated, and the apoptosis marker Caspese-3 phase is up-regulated, suggesting that activating the Wnt/β-catenin signaling pathway increases astrocyte apoptosis and down-regulates the SIRT1 signaling pathway.