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

Fig. 5.

Fig. 5

Effects of 18B12 treatment on colocalization of glial fibrillary acidic protein (GFAP)/tumor necrosis factor (TNF)-α and Iba1/TNF-α after spinal cord injury (SCI). (a, c, l, n) Results are shown for sham-operated mice. (d, f, o, q) Mice with SCI and (g, i, r, t) mice with SCI treated with 18B12. Spinal cord sections were double stained with antibodies against GFAP (a, d, j; green), Iba1 (l, o, r; green), and TNF-α (b, e, h, m, p, s; red). (d, o) Spinal cord sections revealed increased astrogliosis (GFAP + cells) in SCI mice. (g, r) GFAP immunoreactivity was reduced in 18B12-treated mice.(i, t) Yellow spots indicate colocalizations and revealed a high colocalization between GFAP/TNF-α and Iba1/TNF-α double staining