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Fig. 1 | Journal of Neuroinflammation

Fig. 1

From: Type-1 angiotensin receptor signaling in central nervous system myeloid cells is pathogenic during fatal alphavirus encephalitis in mice

Fig. 1

Ang II levels increase in both the brains (a) and spinal cords (b) of mice with NSV encephalomyelitis, while treatment of NSV-infected mice with the ACE inhibitor, captopril, suppresses Ang II induction in the CNS (c) and enhances disease survival (d). Tissue Ang II levels were measured by EIA in homogenates collected from uninfected (day 0) or NSV-infected animals and normalized to the total extracted protein content of each sample. Values measured in individual mice (n = 4–6 samples per time point) and mean concentrations at each time point are shown. One-way ANOVA confirmed that Ang II levels change significantly in both CNS tissue compartments over time (p = 0.0005 for brain, p = 0.0132 for spinal cord). Treatment of mice with captopril (10 mg/kg/day) suppressed Ang II induction on day 3 post-infection compared to mice given a vehicle control (n = 5 samples per group, *p < 0.05 by Student’s t test). This same treatment regimen enhanced overall disease survival compared to mice given a vehicle control (n = 7 mice per group, p = 0.002 using a log-rank (Mantel-Cox) test)

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