NF-κB、IκB、GFAP在脊髓空洞前状态中的表达和作用

目的:脊髓空洞前状态主要表现为脊髓缺血缺氧性水肿,为了探讨其发生的分子生物学机制,观察脊髓组织中的NF-κB、IκB、VEGF、GFAP的表达,探讨它们之间的相互关系。方法:通过枕大池注射Kaolin制作家兔的脊髓空洞症模型,应用免疫组织化学的方法测定不同时间点的脊髓组织中NF-κB、IκB、VEGF、GFAP的表达。结果:Kaolin组动物颈髓组织中,NF—κB表达在术后第1天明显升高,第3天达到高峰,两周时基本恢复正常;IκB各时间点的表达变化与NF-κB成负相关,术后第1天开始明显下降,维持低水平表达至第7天;VEGF主要表达于神经元,神经胶质和血管内皮细胞的胞浆中,术后第1天表达明显增高,第7天达到高峰且维持两周,第3周表达明显减弱,但仍高于正常。GFAP则主要表达于神经胶质细胞,于术后第1天开始升高,但高峰期较VEGF向后延迟至两周并维持到三周仍呈较高水平。结论:在脊髓空洞前状态中,VEGF表达增高,影响BBB的完整性,产生脊髓水肿:GFAP表达增高,代表脊髓组织增强的神经胶质反应。他们二者的高表达同时受NF—κB/IκBα的活性的调节。

Objective: To investigate the roles and mechanism of NF-κB,IκB, VEGF, GFAP in the forming of presyr-inx state of experimental syringomyelia in rabbits, which was composed mainly of hypoxic ischemic edema. Methods: The experi-mental syringomyelia modes of rabbits were established by intra-cisternal injection of kaolin. The expressions of NF-κB,IκB, VEGF, GFAP in spinal cord was measured with imtnunohistochemistry in 1,3,7,14,21d after operation respectively. Results: Comparing with control group, in kaolin group animal, NF-κB expression increased in 1 st day after operation, reached its cosp at 3rd day, and recovered the normal level at 2nd week approximately, IκB expression took negative correlation with NF-κB at the same period, decreased at 1st day markedly and keep this low level to 7 day after operation. VEGF expressed in cytoplasm of the neuron,glia and vascular endothelial cell mainly, its expression increased in 1 st day after operation greatly, reached its cusp at 7 day, and not decreased till the 3rd week; GFAP expressed in glial cell mainly, its expression started to increase at the same time with VEGF, but its cusp phase appear later two weeks than VEGF, and keep this high level for 3 weeks or more. Conclusions: In the presyrix state of experimental syringomyelia, the high VEGF expression may destroy the integrity of BBB, and result to spinal cord edema; GFAP expression upregu-lated play a major role in striking glial proliferation. At the same time, they were regulated by the activity of NF-κB, IκBα.