Figure 6
GCSF decreased p-p38-positive cells in the dorsal horn.
Representative images of double immunofluorescence in the dorsal horn for p-p38 (red) and OX-42, a microglia marker (green; (A)); GFAP, an astrocyte marker (green; (B)); and NeuN, a neuronal marker (green; (C)) of the sham controls, vehicle-treated CCI rats and GCSF-treated CCI rats on the 3rd day after nerve injury. Most p-p38 was co-stained with OX-42-positive cells. (D) Quantification of the OX-42/p-p38-positive cells in the right quarter part of the spinal dorsal horn (lamina I–V) of the sham controls, vehicle-treated CCI and GCSF-treated CCI rats. The vehicle-treated CCI rats had a significantly higher number of OX-42/p-p38-positive cells than the sham control rats on the 3rd day after nerve injury (P < 0.01); in contrast, the GCSF-treated CCI rats had a significantly lower number of OX-42/p-p38-positive cells than the vehicle-treated CCI rats on the 3rd day after nerve injury (P < 0.01). Scale bars = 20 μm. The data are shown as the mean ± SEM. #P < 0.05, ##P < 0.01: GCSF-treated or vehicle-treated groups compared to sham-operated controls. *P < 0.05, **P < 0.01: GCSF-treated CCI groups compared to vehicle-treated CCI groups. Kruskal–Wallis, post hoc Mann–Whitney rank-sum test (n = 5, in each group). Arrowheads indicate OX-42-positive/p-p38-positive cells.
