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目的 研究液压冲击伤后体外培养的大鼠神经元细胞内微管相关蛋白 2 (MAP 2 )的变化 ,探讨尼莫地平 (Nim)、D 2氨基戊酸 (D AP 5 )和亚低温对创伤后MAP 2的影响及机制。方法 通过免疫荧光标记神经元细胞MAP 2 ,利用激光共聚焦显微镜测定液压冲击伤时体外培养的大鼠神经元细胞MAP 2的变化。结果 MAP 2主要位于神经元胞体和树突 ,且树突中MAP 2多于胞体。液压冲击伤后脑皮质神经元细胞MAP 2于伤后 3小时明显丢失 (P <0 0 1) ,4 8小时MAP 2丢失达高峰 ,72小时MAP 2免疫染色部分恢复。Nim于伤后 1小时内应用明显减少MAP 2的丢失 (P <0 0 1) ,而伤后 10小时以上应用则无效 (P >0 0 5 ) ;D AP 5于伤后 10小时内应用明显减少MAP 2的丢失 (P <0 0 1) ;亚低温于伤后 1小时也可减轻MAP 2的丢失 (P <0 0 5 )。结论 液压冲击伤后神经元细胞MAP 2逐渐丢失 ,72h以后部分神经元细胞MAP 2免疫荧光染色部分恢复 ,说明创伤后部分存活神经元微管结构可自行修复。Nim、D AP 5和亚低温通过不同保护机制均可减轻MAP 2的降解 ,但各自应用的时间窗不同 ,提示对创伤后神经元细胞骨架降解应注意综合治疗 ,并选定各自应用的最佳时间窗。
Objective To study the changes of MAP 2 in cultured rat neurons cultured in vitro and the effects of nimodipine (Dim), D 2 aminopentanoate (D AP 5) and mild hypothermia on trauma MAP 2 after the impact and mechanism. Methods MAP2 was detected by immunofluorescence staining and laser scanning confocal microscopy was used to detect the changes of MAP2 in neurons cultured in vitro. Results MAP 2 mainly located in neuronal somatic cells and dendrites, and dendrites MAP 2 more than the body cell. MAP 2 of cerebral cortical neurons was significantly lost at 3 h post-injury (P <0.01), MAP 2 loss peaked at 48 h, and MAP 2 immunoreactivity recovered at 72 h. Application of Nim significantly reduced MAP 2 loss within 1 hour after injury (P <0.01), but no effect was observed more than 10 hours after injury (P> 0.05); D AP 5 was significantly increased within 10 hours after injury Reduce MAP 2 loss (P <0.01). Mild hypothermia also reduced MAP 2 loss 1 hour after injury (P <0.05). Conclusions The MAP 2 in neurons gradually lost after the fluid percussion injury. After 72 h, MAP 2 immunofluorescence staining of some neurons recovered partly, indicating that the microtubule structure of some surviving neurons could be repaired by themselves. Nim, D AP 5 and mild hypothermia can reduce the degradation of MAP 2 by different protection mechanisms, but the different application time windows suggest that comprehensive treatment should be taken for the degradation of post-traumatic neuronal cytoskeleton and the best application of each Time Window.