Fig. 5
Neuronal p47phox deficiency alleviates tau hyperphosphorylation at specific sites in neurons induced by OA treatment. Freshly isolated neurons from WT and Ncf1−/− mice were exposed to OA (10 nM, 25 nM, or 50 nM) for 12 h. a Representative Western blots showing tau hyperphosphorylation at S199, T205, S396, and S404 in primary neurons. b, c Quantification of the immunoreactivity of Western blots, normalized against total tau (Tau5). One-way ANOVA: b, pS199 F (3, 32) = 10.16 p < 0.0001, pT205 F (3, 32) = 5.317 p = 0.0044, pS396 F (3, 32) = 8.480 p = 0.0003, pS404 F (3, 28) = 3.743 p = 0.0223; c, pS199 F (3, 31) = 10.26 p < 0.0001, pT205 F (3, 30) = 22.43 p < 0.0001, pS396 F (3, 31) = 1.171 p = 0.3366, pS404 F (3, 31) = 0.1162 p = 0.9499. Data are mean ± SEM from three separate experiments, each in duplicate or triplicate. *p < 0.05, **p < 0.01, ***p < 0.001, ****p < 0.0001 compared with medium without OA treatment