Fig. 11

P.gingivalis-LPS-induced neuroinflammatory processes via the TLR4/NF-κB signaling pathway. Expression of CD14, TLR4, IRAK1, p65, and p-p65 was measured by western blot analysis (a). Graphs show the semiquantitative analysis of protein levels (b–e). Expression of CD14, TLR4, IRAK1, and p-p65/p65 proteins was upregulated by P.gingivalis-LPS. High expression of these proteins (TLR4, IRAK1, and p-p65/p65) was effectively inhibited by TAK-242. Data are presented as mean ± SEM; *p < 0.05, **p < 0.01, ***p < 0.001, compared to the control group; ^#p < 0.05, ^##p < 0.01, ^###p < 0.001, compared to the P.gingivalis-LPS group