Objective To observe the expression of LIMK1, GFAP and the histological changes after SCI, and to explore whether LIMK1 participate in the formation and control of pathological glial scar. Methods Fifty-four adult Wistar rats were randomly divided into 3 groups： one group was made as control group, one group only accepted the pseudo-operation, the others were made as spinal cord injury （SCI） model by the modified Allen＇s impact device. Locomotor capacity was assessed according to the 21-point Basso, Beanie and Bresnahan score; The lesions were observed with light microscopy and confocal laser scanning microscope at 1, 2, 3 and 4 weeks after SCI. The LIMK1 and GFAP were also observed by immunohistochemistry （IHC） and immunofluorescence assay. Results The mortality rate of SCI group was 33%. BBB scale of hind limb movements showed significant recovery of motor function after SCI in rats （P〈0.01）. There is a high degree of concordance between IHC and laser scanning confocal analysis for LIMK1 and GFAP. Both of the protein expression level increased at 1 week after SCI. The expression of GFAP reached the peak at 3 weeks after injury, and began to fail at 4 weeks. The peak of LIMK1 showed immediately at 1 week, then dropped at 2 weeks. But another peak was formed at 3 weeks and began to fail at 4 weeks. Conclusion After spinal cord injury, the expression of LIMK1 and GFAP are closely related. The expression profile of LIMK1 suggests that LIMK1 may play an important role in the glial scar development.