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. 2016 May 23;13(4):880–894. doi: 10.1007/s13311-016-0446-2

Fig. 4.

Fig. 4

Effects of 18B12 treatment on astrocyte activation and tumor necrosis factor (TNF)-α expression in spinal cord tissue. Spinal cord sections were processed to determine the immunohistologic staining for glial fibrillary acidic protein (GFAP) and TNF-α expression. (a, g) No positive staining for TNF-α was found in the spinal cord tissue from the sham group. (b, g) TNF-α expression increased in spinal cord tissues from spinal cord injury (SCI) mice 24 h after SCI. (c, g) 18B12 treatment significantly attenuated TNF-α levels in the spinal cord. (d, g) Moreover, sham animals never expressed GFAP, but (e, g) the number of GFAP+ cells was significantly increased after induction of SCI. (f, g) 18B12 significantly decreased the activation of astrocyte GFAP+ cells. The figure is representative of at least 3 experiments performed on different experimental days. Data are expressed as percentage of total tissue area. Data are mean ± SEM of 10 mice from each group. ### p < 0.001 vs sham; ***p < 0.01 vs SCI ND = not detectable