The Effects Of Vertebral Canal Decompression On Neural Apoptosis Induced By Compressive Spinal Cord Injury In The Rats

Objective :To investigate the changes of Ire1α,Caspase-12 and Caspase-3 expression in the vertebral canal decompression following compressive spinal cord injury , so as to clarify the effects of decompression on neural apoptosis induced by compressive injury of rat spinal cord.Methods : Fifty adult Sprague-Dawley rats (240-300g) were randomly divided into 2 groups, including shame-operation group (n=10) and operation group (n=40). The spinal cord was compressed posteriorly at L1 level using a self-designed device for 1,6, 12 and 24 h, followed by decompression by removal of the screw. Apoptosis and cellular damage of the compressive segments were assessed by the staining of HE,Nissl,terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling(TUNEL), immunohistochemistry,Western blotting and image analysis.Results :HE and Nissl staining showed the edema of neurons and gliocytes,reduction of processes,vacuolation and spongy degeneration in the white matter of the injury spinal cord after 6 h of compression. Immunohistochemistry detection and Western blotting indicated that the expression of Ire1αand Caspase-12 was increased in the decompression at 1 h after spinal cord injury,and peaked at 24 h. The number of Caspase-12 positive neurons in the decompression at 1,6,12,24 h groups was (19.71±1.43),(29.45±1.18),(44.11±2.46) and (81.46±1.13),which was significantly higher than that of the shame-operation group (P<0.05). Caspase-3 immunoreaction was consistent with the changes of Tunel positive neural cells.Conclusions :Increased expression of Caspase-12 indicates that there was an endoplasmic reticulum stress in the spinal cord compressive injury;Ire1αmay play an important role in the neuronal apoptosis. The dynamic change of apoptosis was correlated with the duration of spinal compression. Early decompression could reduce neural cell apoptosis following secondary spinal cord injury.