摘要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＜0.01)，48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＜0.01)，而伤后10小时以上应用则无效(P＞0.05)；D-AP-5于伤后10小时内应用明显减少MAP-2的丢失(P＜0.01)；亚低温于伤后1小时也可减轻MAP-2的丢失(P＜0.05)。结论液压冲击伤后神经元细胞MAP-2逐渐丢失，72 h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。

abstractsObjective To investigate alterations in the microtubule-associated protein 2 (MAP-2) of neurons in Wistar rats and the effect of nimodipine (Nim), D-2-amino-5-phosphonovaleric acid (D-AP-5) and mild hypothermia on neuronal MAP-2 following fluid percussion injury (FPI).Methods Alterations of MAP-2 in Wistar rat neurons following FPI were measured by a confocal laserscanning microscope using MAP-2 immunofluorescence staining as a MAP-2 indicator.Results MAP-2 immunofluorescence staining was limited to the cell bodies and dendritic compartments of neurons and more intense in dendrites than in cell bodies. The loss of MAP-2 was marked at 3 h posttrauma ( P ＜ 0.01 ), and reached a maximum at 48 h post-trauma. Afterwards, fluorescence recovered partly at 72 h post-trauma. The application of Nim markedly reduced the loss of MAP-2 immunoreectivity within 1 h post-trauma ( P ＜ 0.01 ), and the application of D-AP-5 markedly reduced the loss of MAP-2immunoreactivity within 10 h post-injury ( P ＜ 0.01 ). The application of mild hypothermia decreased the loss of MAP-2 immunoreactivity within 1 h post-injury (P＜ 0.05).Conclusions The partial recovery of fluorescence at 72 h post-trauma indicate that the partial structure of the neuronal microtubules can be repaired by itself. Nim, D-AP-5 and mild hypothermia reduce the degradation of MAP-2 by different mechanisms. The treatment of neuronal cytoskeleton degradation following FPI must employ multiple therapeutic approaches.