Chinese Journal of Tissue Engineering Research ›› 2016, Vol. 20 ›› Issue (5): 640-645.doi: 10.3969/j.issn.2095-4344.2016.05.006

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Propofol intervention affects spinal cord edema and hindlimb electrophysiology in a model of spinal cord injury

He Jue1, Wang Tian-ke2
  

  1. 1Department of Pathology, Gannan Medical University, Ganzhou 341000, Jiangxi Province, China; 2Department of Pathology, Affiliated Cixi Hospital of Wenzhou Medical University, Ningbo 315300, Zhejiang Province, China
  • Received:2015-11-17 Online:2016-01-29 Published:2016-01-29
  • About author:He Jue, Associate professor, Department of Pathology, Gannan Medical University, Ganzhou 341000, Jiangxi Province, China

Abstract:

BACKGROUND: A large number of studies have verified that propofol could effectively reduce secondary nerve injury by improving microenvironment of spinal cord injury.
OBJECTIVE: To study the effects of propofol on spinal cord edema and electrophysiology of the hind limb in rats with spinal cord injury.
METHODS: Rat models of acute spinal cord injury were established by using the modified Allen method. A total of 40 rat models were randomly divided into spinal cord injury group and propofol group (n=20). Rats in the propofol group were injected with propofol through the caudal vein. The spinal cords of an additional 20 rats were exposed in the sham surgery group. Motor function was evaluated using BBB score and inclined plate test before modeling, 1, 3 days, 1-4 weeks after modeling. Neuronal apoptosis was detected after spinal cord injury using TUNEL assay at 72 hours after modeling. AQP4/9, matrix metalloproteinases 9/2 mRNA and protein expressions were measured using RT-PCR and western blot assay. At 4 weeks after modeling, pathological changes of the spinal cord were observed using immunohistochemistry and hematoxylin-eosin staining. Neurophysiological recovery was analyzed using motor evoked potentials and somatosensory evoked potentials.
RESULTS AND CONCLUSION: (1) At 1-4 weeks after modeling, BBB score and inclined plate test score were higher in the propofol group than in the spinal cord injury group (P < 0.05), but lower than in the sham surgery group (P < 0.05). (2) The number of apoptotic cells was significantly more in the spinal cord injury group than in the propofol group (P < 0.05). No apoptotic cells were found in the sham surgery group. (3) At 72 hours after spinal cord injury, AQP4/9 and matrix metalloproteinases 9/2 mRNA and protein expression was higher in the propofol group than in the sham surgery group (P < 0.05). AQP4/9 and matrix metalloproteinases 9/2 mRNA and protein expression was significantly reduced in the propofol group (P < 0.05). (4) At 4 weeks after modeling, the spinal cord was loose, and the cavity was small. Partial neuronal necrosis could be seen. The degree of nerve fiber density in the propofol group was between the sham surgery group and spinal cord injury group. (5) Motor evoked potentials and somatosensory evoked potentials were obviously recovered, the latency was short, amplitude was increased in the propofol group, which showed significant differences as compared with the sham surgery group and the spinal cord injury group (P < 0.05). Results suggested that propofol can reduce apoptosis in rat neurons after spinal cord injury, reduce spinal cord edema-related gene expression, and improve electrophysiological function and limb motor function.