Fig. 8

Nox subunits are upregulated in the CNS following NSV challenge (a, b), and enzymatic activity capable of generating ROS is both induced in the brains (c) and spinal cords (d) of infected animals and inhibited by telmisartan as well as by genetic deletion of Nox subunits. Normalized gp91 and p47 expression in whole tissue extracts was determined by Western blot as described in the “Methods” section. One-way ANOVA confirmed that levels of both Nox subunits changed significantly in both CNS regions over time (p < 0.0001). ROS-generating enzyme activity was measured directly in tissue extracts as described in the “Methods” section. Values derived from individual mice as well as mean enzyme activity levels are shown for each experimental condition (n = 5 mice/group). Student’s t test was used to analyze the degree to which telmisartan (100 mg/kg/day) or Nox subunit deletion suppressed enzyme activity in tissues derived from NSV-infected animals compared to those from vehicle-treated controls (*p = 0.0009 in brain and p = 0.0026 in spinal cord; **p = 0.0005 in brain and p = 0.0004 in spinal cord)