Fig. 7

EVT901 treatment attenuated the infiltration of peripheral monocytes/macrophages into the injured brain in WT mice. a Brain tissue sections from C57BL/6 mice at 7 days after TBI were immuno-stained with CD45 and F4/80 Abs. b TBI increased the proportional area of CD45 + F4/80+ double-positive signal in the injured brain, while EVT901 treatment reduced it. ANOVA indicated that there was a significant treatment effect (F _1,6 = 14.89, p = 0.005, η ² = 0.83, power = 0.97). Tukey’s post hoc test revealed a significant difference between uninjured vs TBI-vehicle (^## p = 0.004) and TBI-vehicle vs TBI-EVT901 (**p = 0.006). c–f Cells isolated from C57Bl/6 WT mice brains at 1 and 6 weeks after sham or TBI, with or without EVT901, were stained with Abs against CD45, CD11b+, and F4/80. c, d TBI increased the absolute number of CD45^highF4/80+ monocytes, and EVT901 significantly reduced the number. Two-way ANOVA followed by Tukey’s post hoc tests showed that there was a significant effect of condition (F _3,36 = 4.06, p = 0.016, η ² = 0.31, power = 0.779), but no effects of time. TBI increased CD45^highF4/80+ cells in the injured brain compared to sham, while EVT901 treatment abrogated this effect (*p < 0.05). e, f TBI significantly increased the absolute number of CD45^highCD11b+ monocytes in the injured brain, and EVT901 significantly reduced it. Two-way ANOVA showed a significant effect of condition (F _3,35 = 9.02, p = 0.0002, η ² = 0.5, power = 0.99), but no effect of time. Tukey’s post hoc tests showed a significant effect of injury and EVT901 at both 1 and 6 weeks (*p < 0.05, **p < 0.001 compared to TBI-vehicle). Scale bar in A = 1000 (left) and 100 μm (right). (n = 3–4 for sham and n = 5–7 for TBI)