中文摘要：

目的 研究不同强度磁刺激对星形胶质细胞迁移作用的量效关系,并探讨其作用机制.方法 24只SD大鼠按刺激强度被随机分为A（O T）、B（1.9 x40%T）、C（1.9×80%T）、D（1.9×100%T）4组,4组的刺激频率均为1 Hz,刺激量为30个脉冲,均采用溴已锭（EB）注入脊髓左侧背索复制局灶性的脊髓损伤模型.刺激后第14天,处死大鼠,采用图像分析系统观察胶质纤维酸性蛋白（GFAP）、微管相关蛋白-2（MAP-2）和细胞外信号调节激酶1/2（ERK1/2）的表达及脊髓损伤区空洞体积的变化.结果 随着磁刺激强度的增加,在第14天时空洞的体积逐渐缩小,组间差异具有统计学意义（P〈0.05）.在空洞缩小的区域中,可以观察到GFAP,ERK1/2的阳性表达,而无MAP-2的阳性表达.随着磁刺激强度的增加,GFAP,ERK1/2的阳性表达亦显著增强（P〈0.05）.结论 磁刺激可影响星形胶质细胞的迁移,并随着刺激强度的增强,星形胶质细胞迁移的能力亦增强,这可能与ERK1/2的高表达有关.

英文摘要：

Objective To investigate the effect of magnetic stimulation on astrocyte migration and its mech- anism. Methods Twenty-four adult, healthy Sprague-Dawley rats were injected with 0. 5μl of 1% ethidium bro- mide （EB） in the left side of the dorsal spinal cord funiculus at the T10-11 level to make a local spinal cord injury mod- el. They were then randomly divided into four groups and exposed to 30 pulses of magnetic stimulation at 1 Hz and the following intensities： 0 T （Group A）;1.9 ×40% T （Group B）; 1.9 ×80% T （Group C）; 1.9 × 100% T （Group D）. On the 14th day after stimulation, the rats were sacrificed and the expression of glial fibrillary acidic protein （GFAP）, mierotubule associated protein-2 （MAP-2） and extracellular signal-regulated kinase 1/2 （ERK 1/2） were detected, and the volume of holes in the injured area of the spinal cord was measured. Quantitative analysis of the GFAP, MAP-2 and ERK1/2 expression was performed using immunohistoehemistry and an image anal- ysis system. Results The volume of holes in the injured area of the spinal cord decreased with increasing stimula- tion intensity. In the reduced area of the holes, the expression of GFAP and ERK 1/2 could be seen, but not MAP-2. Significant differences were revealed in the expression of GFAP and ERK 1/2 among the four groups, but it was always significantly higher in the magnetic stimulation groups than in the controls. Conclusions After magnetic stimulation, astrocytes migrate into the injured spinal cord＇s holes. Astrocyte migration increases with increased magnetic stimulation intensity, which may be associated with high expression of ERK 1/2.