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. 2020 Mar 11;40(11):2357–2370. doi: 10.1523/JNEUROSCI.2516-19.2020

Figure 6.

Figure 6.

IFN-β deficiency reduces lesion volume and hippocampal neurodegeneration after TBI. Immunofluorescence analysis of NOX2 (green) and CD68 (red) demonstrates that injury-induced NOX2 expression in reactive microglia/macrophages was significantly decreased in IFN-β−/− TBI mice compared with WT TBI mice at 28 dpi (A). Scale bar, 50 μm. Representative images of cresyl violet stained coronal sections from WT and IFN-β−/− TBI mice at 28 dpi (B). Quantification of lesion volume in WT and IFN-β−/− TBI mice at 28 dpi. IFN-β−/− resulted in a significant reduction in TBI lesion volume (p = 0.003, B). Quantification of hippocampal neurodegeneration in WT and IFN-β−/− TBI mice at 28 dpi (C). In WT mice, TBI resulted in significant loss of hippocampal neurons compared with the WT sham group. In contrast, TBI in IFN-β−/− mice resulted in reduced neuronal loss, which was significantly different to the WT TBI group. Data expressed as mean ± SEM. ***p < 0.001 vs sham (effect of TBI) and +++p < 0.001 WT TBI vs IFN-β−/− **p = 0.0013 (Sham WT vs WT TBI), +p < 0.05 WT TBI vs IFN TBI. A, Two-way ANOVA (n = 4–5/group), B, Student's t test (n = 6–7/group), and C, Two-way ANOVA (n = 4–5/group).