Fig. 8.

Systemic administration of altenusin (2 and 10 mg/kg) at 30 minutes postinjury. Mice were euthanized and perfused after 24 hours, and cortical tissue was processed for mRNA analysis (A). Gene expression of proinflammatory molecules were analyzed in the cortex of sham, vehicle, and altenusin administered TBI mice (vehicle-treated CCI significantly induced expression of proinflammatory mediators, TNF-α (B), IL-6 (C), IL-1β (D), iNOS (E) CCL2 (F), and microglia activation marker CD68 (G), reactive oxygen species (ROS) inducer NOX2 (H) and p22-phox (I), compared with sham-treated animals. Altenusin treatment (10 mg/kg) significantly reduced expression of all above mentioned genes. Analysis done by one-way ANOVA, followed by post hoc adjustments using Tukey’s multiple comparison test. Results are expressed as means ± S.E.M. (N = 5–7 animals each group). *P < 0.05, **P < 0.01 in comparison with TBI (vehicle); ^##P < 0.01, ^###P < 0.001 in comparison with sham.