高压氧对大鼠脊髓损伤后血管内皮生长因子表达的影响

目的通过观察高压氧对成年大鼠脊髓损伤后不同时期血管内皮生长因子（VEGF）表达变化的影响,探讨高压氧对脊髓损伤的治疗作用机制。方法雌性SD大鼠55只,体质量250-300g。随机分为脊髓损伤组（对照组）、脊髓损伤＋高压氧治疗组各25只（n=5）,假手术组5只。采用改良A llen＇s法制作T8脊髓打击伤动物模型,各组分别于伤后1 d、1 w、2 w、4 w和8 w进行行为学观察,运动功能评分方法（BBB）评分后损伤部位取材,免疫组化染色及图像分析检测组织中VEGF的表达。结果假手术组的评分21分,治疗组和对照组与假手术组比较在各时间点评分明显降低,治疗组在各时间段BBB评分明显高于对照组（P〈0.05）。假手术组显示除脊髓中央管周围可见到极少量VEGF表达外,其它部位几乎不表达;对照组脊髓损伤1 d VEGF在大鼠脊髓损伤区及损伤周边区高表达,主要出现在软脊膜和脊髓灰、白质血管壁上的血管内皮细胞胞浆内,脊髓灰、白质内的神经胶质细胞和巨噬细胞胞浆内也出现表达,一般脊髓白质中更为多见,1 w后下调,而治疗组1 d至2 wVEGF的表达较对照组明显增加,差异有显著性（P〈0.05）,4 w、8 w时各组比较无统计学差异。结论急性脊髓损伤可上调VEGF在脊髓血管内皮细胞、胶质细胞和巨噬细胞内的表达,高压氧可能通过促进VEGF表达,促进血管内皮细胞生长从而对脊髓损伤起到治疗作用。

Effect of hyperbaric oxygen on expression of VEGF after spinal cord injury in rats

Objective To study the effect of hyperbaric oxygen （HBO） on expression of vascular endothelial growth factor （VEGF） after spinal cord injury （SCI） in rats at different time and to investigate the curative mechanism of HBO on SCI. Methods Fifty-five female adult Sprague-Dawley rats, weighing from 250 to 300 g, were divided into 3 groups randomly： control group （25, n =5）, hyperbaric oxygen therapy group （25, n =5） and normal group （5, n = 5）. In the experimental groups, the rat spinal cord injury models were established by Allen＇s method and the expressions of VEGF at different time （1 day, 1 week, 2 week, 4 week, 8 week ） were observed with immunohistochemical staining and the analytical system of photographs. Results In the normal group, the expression of VEGF could hardly be seen except ependymal cells of central canal. In the experimental groups, the expression of VEGF increased obviously in the injured sites and adjacent sites 1 d to 1 w after injury, reached the peak after 1 w and followed by a gradual decrease from 1 w to 2 w. There was statistical significant difference in the expression of VEGF between the hyperbaric oxygen therapy group and the control group. Conclusion The spinal cord injury can induce the expression of VEGF. HBO may perform the therapeutic effect on SCI by the maintenance and induction of growth of vascular endothelial cells through enhancing the expression of VEGF.