Fig. 4

The regulation of FTS•B on proteins related to neuroinflammation in the hippocampus of APP/PS1 mice. (a) FTS•B reduced the expression levels of JIP3 and the phosphorylation levels of JNK and APP. (b) FTS•B suppressed the expression levels of ELKS and the phosphorylation levels of IKK(α + β), IκBα, and NF-κB p65. (c) FTS•B enhanced the expression levels of WDFY1 and TLR3, as well as the phosphorylation levels of IRF3. (d) FTS•B reduced the expression levels of Iba1 and GFAP. Quantification data were normalized to GAPDH and corresponding total proteins (n = 3). They were reported as folds of the corresponding WT group. FTS•B, forsythoside B; APP/PS1, amyloid precursor protein/presenilin 1; JIP3, JNK-interacting protein 3; JNK, C-Jun NH2-terminal kinase; APP, amyloid-beta precursor protein; IKK, inhibitor of nuclear factor kappa-B kinase; IκBα, inhibitor of nuclear factor kappa-B alpha; NF-κB, nuclear factor-κB; WDFY1, WD-repeat and FYVE-domain-containing protein 1; TLR3, toll-like receptor 3; IRF3, interferon regulating factor 3; Iba1, ionized calcium-binding adapter molecule 1; GFAP, glial fibrillary acidic protein