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 Alen 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 metaloproteinases 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 cels was significantly more in the spinal cord injury group than in the propofol group (P < 0.05). No apoptotic cels were found in the sham surgery group. (3) At 72 hours after spinal cord injury, AQP4/9 and matrix metaloproteinases 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 metaloproteinases 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 smal. 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.%背景：大量研究证实，丙泊酚通过改善脊髓损伤的微环境，可以有效减少继发性神经损伤。目的：探讨丙泊酚干预对脊髓损伤大鼠脊髓水肿和后肢电生理的影响。方法：按照改良的Al en打击法形成大鼠急性脊髓损伤模型，取建模成功40只大鼠随机分为脊髓损伤组和丙泊酚组，每组20只，丙泊酚组尾静脉泵注丙泊酚。另20只假手术组大鼠只暴露脊髓组织。分别于造模前、造模后1，3 d与1-4周通过BBB评分、斜板实验进行运动功能评定。造模后72 h采用TUNEL法检测脊髓损伤神经元凋亡情况，RT-PCR和Western blot法检测脊髓组织水通道蛋白4/9、基质金属蛋白酶9/2 mRNA和蛋白的表达。造模后4周进行免疫组化和苏木精-伊红染色观察脊髓组织病理变化，运动诱发电位和体感诱发电位分析大鼠神经电生理恢复情况。结果与结论：①造模后1-4周，丙泊酚组BBB评分、斜板实验评分均高于脊髓损伤组(P <0.05)，但均较假手术组低(P <0.05)。②脊髓损伤组凋亡细胞数明显多于丙泊酚组(P <0.05)，假手术组没有凋亡细胞。③脊髓损伤后72 h，丙泊酚组损伤区脊髓组织水通道蛋白4/9、基质金属蛋白酶9/2 mRNA和蛋白表达高于假手术组(P <0.05)；丙泊酚组大鼠损伤区脊髓组织水通道蛋白4/9、基质金属蛋白酶9/2 mRNA和蛋白的表达较脊髓损伤组明显减少(P <0.05)。④造模后4周，丙泊酚组脊髓损伤区组织较为疏松，脊髓空洞较小，可见部分神经元坏死，丙泊酚组神经纤维密集程度介于假手术组与脊髓损伤组之间。⑤丙泊酚组运动诱发电位和体感诱发电位明显恢复，潜伏期缩短，波幅增高，与假手术组和脊髓损伤组比较差异有显著性意义(P <0.05)。⑥结果表明丙泊酚能够减少脊髓损伤后神经元细胞凋亡，降低脊髓水肿相关基因表达，改善电生理功能及肢体运动功能。
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