摘要:
目的：观察神经节苷脂(GM1)对脑外伤大鼠大脑皮质中Nogo-A表达的影响，探讨GM1促进脑外伤神经修复的可能机制。方法：采用SPF级SD大鼠100只，随机分为空白对照组(n=10)、假手术组(n=20)、损伤后生理盐水组(n=35)和损伤后GM1组(n=35)。通过HE染色观察各组大鼠脑组织不同时间点病理情况；用免疫组化的方法观察Nogo-A阳性细胞数量。结果：通过免疫组化的方法观察损伤后生理盐水组：Nogo-A阳性细胞在造模24时即明显升高，至72h时仍呈升高的趋势；GMl组:Nogo-A的阳性细胞数早期逐渐升高，至24h时数量最多，之后开始减少，应用GMl后，Nogo-A的阳性细胞数量的增加较为延后。结论：Nogo-A在颅脑损伤后其阳性细胞数量显著增高，抑制中枢神经损伤后的再生，神经节苷脂GM1在脑损伤后可部分抑制Nogo-A的表达，机制可能通过稳定细胞膜、减轻细胞水肿，从而发挥对实验性脑外伤大鼠的神经保护作用。
Abstract:
Objective: To observe the effects of the ganglioside (GM1) on Nogo-A expression in cerebral cortex for the rats which have brain trauma, to explore the possible mechanisms of GMl promoting the nerve repair of traumatic brain injury. Methods: SPF SD rats of 100 were randomly divided into four groups: no operation group (n=10), sham operation group (n=20), saline model group (n=35), GMI group (n=35). ELISA was used to detect Nogo-A expression in parietal cerebral cortex at different time. Results: By immunohistochemical method we observed in model group: the number Nogo-A positive cells increased at 24 hours in the model, and still slightly increased till 72 hours; in group GM1: the number Nogo-A of positive cells increased gradually in the early time, and became largest at24 h, then started to decrease, the application of GM1, after brain trauma, the increase in the number of Nogo-A positive cells was more delayed. Conclusions: the number of Nogo-A positive cells increased significantly after brain trauma, and inhibited the CNS regeneration after injury. After brain trauma, the ganglioside GM1 partially inhibited Nogo-A expression, and the mechanism might be through the stability of cell membrane, which played its neuroprotection roles in experimental traumatic brain injury in rats.