Tau Antibody - #AF6141

Figure 3. Effects of rPVL on the regulation of RhoA/ROCK/LIMK/Cofilin and PI3K/AKT/GSK-3β signaling pathways and phosphorylation of cofilin and tau hyperphosphorylation in the rPVL-treated BMECs. Representative immunoblot bands for RhoA, p-ROCK2(Tyr722), ROCK2, p-LIMK1/2(Thr508/Thr505), p-cofilin (Ser3), and cofilin (A); p-PI3K (Tyr458/Tyr199), PI3K, p-AKT(Ser473), AKT, GSK-3β(Ser9), GSK-3β, p-tau (Ser396), and tau (B); GAPDH was used as a control. rPVL was used at a 100 ng/mL concentration. Data are expressed as mean ± standard deviation of three independent experiments. * 0.01 < p < 0.05, ** p < 0.01 (one-way ANOVA with Dunnett’s multiple comparison tests), ns: not significant.

Figure 9. |Effect of Nrf2 siRNA on p62, p21, and p-tau/tau protein expression levels in PC12 cells. (C,D) After transfection with 20 µM of Nrf2 siRNA, cells were then pre-treated with Andro (20 µM) for 1 h followed by stimulation with Aβ (10 µM) for an additional 24 h. Then, p62, p21, and p-tau/tau protein expression levels were evaluated by Western blot analysis. * p < 0.05 versus the blank control;# p < 0.05 versus Andro+Aβ1–42 group were considered statistically significant differences.

FIGURE 6 Cognitive function was evaluated with the novel-object recognition test (A) and the Barnes maze test (B). In both trials, TBI-HT and TBI-NT rats showed impaired cognitive performance compared with sham controls (*p < 0.05, TBIs vs. sham and TBI-HT vs. TBI-NT, n = 8–12 animals per group). Posttraumatic cognitive impairment was exacerbated in the hypothermic TBI rats compared with the normothermic TBI rats (**p < 0.05 TBI-HT vs. TBI-NT, n = 12 animals per group). (C) Western blot analysis shows obvious beta-amyloid and p-tau accumulation in rat brains 1 month after TBI and hypothermia. Quantitative analysis shows significantly increased β-amyloid (D) and p-tau (E) deposition in TBI-HT and TBI-NT rats compared with sham controls (Mean ± SD, one-way ANOVA with Bonferroni’s post-hoc test for multiple comparisons; n = 4–6 animals per group, n.s.: not significant). The correlation between p-tau and β-amyloid accumulation with glymphatic dysfunction and cognitive deficits is described in box plot graphs (F–H). Box plot graphs (F) show that the amyloid β and p-tau levels in the brains of sham control, TBI-NT, and TBI-HT rats were inversely linearly related to the reduced influx and efflux rate and linearly related to the increased clearance constant of high-molecular-weight contrast transported along with perivascular spaces (pineal and pituitary recess and periarterial space of the olfactory artery) in the four groups (r2 = 0.94, 0.92, 0.93 for amyloid β level and r2 = 0.90, 0.89, 0.91 for tau level and the influx rate, efflux rate and clearance constant, respectively, all p < 0.01, Spearman’s correlation test, n = 20). Scatter plot graphs (G,H) show that the amyloid β and p-tau levels in the brains of the four groups are linearly related to their increased mean escape time in the Barnes maze test (amyloid β: r2 = 0.96, p-tau: r2 = 0.95, p < 0.01, Spearman’s correlation test, n = 20) and inversely linearly related to their decreased discrimination index in the novel object recognition test (amyloid β: r2 = 0.97, p-tau: r2 = 0.94, p < 0.01, Spearman’s correlation test, n = 20).

Figure 4. The cholinergic and GABAergic neurons were increased by up-regulated the LHX8 in the HSHF diet offspring when they getting older. (A) The mRNA sequence of whole brain tissues; (B, C) the cholinergic and GABAergic cells marked protein of ACEh, Amp, CHRNA1, CHRNB1 and GAD65; the synaptic functional markers of Dynamin 1 and PSD95, and the AD biomarkers of Tau, p-Tau, APOE, CD33 and TREM2 (D). The KEGG analysis results see in the Supplementary Figure 6. Data are presented as the means ± SD of more than 3 independent experiments in Western bolting. *p