Figure 4

The roles of gp91^phox in superoxide radical production after traumatic brain injury). (A) Superoxide radical production (hydroethidium [HEt]-positive cells: shown in red) in the peri-contusional area of wild type (upper) and gp91^phox-/- (lower) mice 2 days after TBI. (B) TBI-induced superoxide radical production (HEt-positive cells) in the peri-contusional area was significantly attenuated by gp91^phox deficiency in sham-operated mice, and 2 days after TBI (*p < 0.05, t test). All values represent mean ± SE. (C, D) Co-localization of HEt-positivity with cell markers in the peri-contusional region. Cell identification was carried out using antibodies for gp91^phox (C), CD11b (D, left), GFAP (D, middle), and Neu N (D, right) (shown in green). HEt-positive cells were co-localized with gp91^phox-positive cells (C, right, arrows) and microglia-like cells (D, left, arrows). Although HEt-positive cells were also slightly co-localized with neurons (D, right, arrows), immunoreactivity was lower than for gp91^phox-positive cells and microglia-like cells. Cells were counter-stained with DAPI to show nuclei (blue). Scale bars = 20 μm (C, D).