Fig 1: RI and RCI induce mouse blood–brain barrier (BBB) leakage. Levels of ICAM1 and GFAP in mouse brain tissue and serum from sham-irradiated control, skin wound, RI, and RCI mice were measured via ELISA (N = 4–5/group). Data are presented as means ± SD. * p< 0.05; ** p < 0.01 vs. sham-irradiated control group. Wound: skin wound; RI: 9.5 Gy; RCI: 9.5 Gy + SW.
Fig 2: RI and RCI induce microglial, endothelial cell, and astrocyte activation. (a) Mouse brain tissues were collected from left brain, right brain and hindbrain 30 days after TBI. The microglial activation marker MHC-II, the astrocyte activation marker GFAP, and the neuro-endothelial cell activation marker ICAM1 were examined via immunoblotting. Data are presented from one of two independent experiments. (b–e) Immunohistochemistry (IHC) staining of brains with anti-GFAP and anti-ICAM1 antibodies. Mouse brain specimens from sham-irradiated control, SW, RI, and RCI were stained with (b) anti-GFAP or (d) anti-ICAM1; scale bar = 25 µm. Brown color indicates positive staining and IgG control antibodies show negative staining. Quantification of GFAP IHC staining is shown in (c) and ICAM1 IHC staining is shown in (e). Three animals/group and two slides/animal. Data are presented as means ± SD. ** p < 0.01 vs. sham control group. Note that RCI group has the highest % of GFAP- and ICAM1-positive cells, with an enlarged cell size. SW or Wound: skin wound; RI: 9.5 Gy; RCI: 9.5 Gy + SW.
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