Skip to main content
. 2015 Oct;185(10):2641–2652. doi: 10.1016/j.ajpath.2015.06.016

Figure 5.

Figure 5

Neutrophil and macrophage density and apoptosis increase in liver after brain injury. A: The number of neutrophils [myeloperoxidase (MPO)-positive cells] was lower in liver from control mice compared with in liver from injured mice treated with vehicle, and injured mice treated with telmisartan (Telm). High-power images show hepatic cells with MPO marker (red) and nuclei with DAPI (blue). B: Telmisartan did not reduce the number of neutrophils infiltrating the liver that were induced by cortical impact injury (CCI). C: Images of terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling (TUNEL)–positive cells (green) in a single field for control, injured mice treated with vehicle, and injured mice treated with Telm. High-power images show apoptotic cells with the TUNEL marker (green) and nuclei with DAPI (blue) for the vehicle group. D: Telmisartan did not reduce the number of TUNEL-positive cells in the liver that were induced by CCI. E: Immunofluorescence staining of CD68-positive macrophages (red) in liver with nuclei stained with DAPI (blue). F: Macrophages in the liver increase after CCI, but telmisartan treatment does not reduce the number of CD68-positive cells. Data are expressed as means ± SEM (B, D, and F). n = 5 to 8 per group (B, D, and F). ∗P < 0.05, ∗∗∗P < 0.001, and ∗∗∗∗P < 0.0001 comparing liver from injured mice and control mice. Scale bars: 50 μm (A, C, and E, ); 20 μm (A, C, and E, high-magnification images in the insets).