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

Figure 4.

Figure 4

Serum amyloid A1 (SAA1) protein expression in liver is induced after brain injury and reduced after telmisartan (Telm) treatment. Representative Western blot analyses showing SAA1 monomers and SDS-resistant SAA1 species in liver homogenates after ultracentrifugation (in dissolved pellet fractions). A: Cortical impact injury (CCI) increases the amount of SAA1 monomers, but not SDS-resistant SAA1 species, in livers of injured mice. Quantification of SAA1 protein expression normalized to that of β-actin. Averages were calculated from three independent replicates. B: SAA1 protein is up-regulated, with a peak of expression at 1 day post-injury (dpi), decreasing at 3 dpi, and returned to control (C) levels by 30 dpi. C: Representative Western blot analyses showing SAA1 monomers (12 kDa) at 3 dpi (duplicate samples). D: Telmisartan (1 mg/kg) significantly reduces SAA1 expression compared with mice treated with vehicle at 3 dpi. E: Immunohistochemical staining of SAA1 (green) and DAPI (blue) in mice liver from control group showing low expression of SAA1; liver tissue from brain-injured, vehicle-treated mice display a significant increase in SAA1 immunofluorescence in the cytoplasm of hepatocytes. Treating brain-injured mice with telmisartan significantly reduces SAA1 immunofluorescence. F: Quantification of immunofluorescence of SAA1 expression shows low SAA1 fluorescence intensity in naïve mice that is increased after 3 dpi. Mice treated with telmisartan after brain injury exhibit a decrease in SAA1 fluorescence intensity. Values are expressed as means ± SEM (B, D, and F). n = 5 to 8 per group (B, D, and F). ∗P < 0.05, ∗∗P < 0.005, and ∗∗∗P < 0.001.