Fig. 9

Acute inhibition of NOX2 using gp91ds-tat alters microglia/macrophage polarization marker expression. Protein samples (25 μg) were probed for CD206, iNOS, CD86, and GAPDH at 24 h, 7 days, and 28 days post-injury in naïve (n = 8), scrambled ds-tat- (n = 4/24 h; 6/7 days; 3/28 days), and gp91ds-tat-treated samples (n = 4/24 h; 5/7 days; 3/28 days). Pixel densitometry for CD206 (a), CD86 (b), and iNOS (c) showed significant alteration with gp91ds-tat treatment in comparison to scrambled ds-tat treatment. The M2 marker CD206 was elevated in both groups at 24 h in comparison to naïve, but remained elevated only in the gp91ds-tat-treated group at 7 days post-injury, before returning to baseline levels by 28 days. In contrast, at 24 h, the inhibition of NOX2 significantly reduced the expression of the M1 marker CD86, although by 7 and 28 days, no significant difference was observed between groups. Finally, a second M1 marker, iNOS, was elevated in both groups at 24 h post-injury, and gp91ds-tat treatment only prevented this induction by 7 days post-injury. *p < 0.05 vs naïve; +p < 0.05 vs scrambled; one-way ANOVA with Tukey’s post-test. Bars represent mean ± SEM