Fig. 2

FTS•B ameliorated pathological alterations in the brains of APP/PS1 mice. FTS•B alleviated the deposition of Aβ in the brains of APP/PS1 mice, detected using (a) thioflavine S staining in the hippocampus and cortex (100×; scale bar: 100 μm; n = 3) and (b) immunohistochemistry in the hippocampus (40×; scale bar: 200 μm; 200×; scale bar: 50 μm; n = 3). FTS•B reduced the levels of (c) phospho-tau protein (n = 3), (d) 4-HNE (n = 3), and (e) GFAP (n = 3) in the hippocampus of APP/PS1 mice (40×; scale bar: 200 μm; 200×; scale bar: 50 μm). (f) FTS•B suppressed the enrichment of Iba1 around blood vessels in the hippocampus of APP/PS1 mice (n = 3; 40×; scale bar: 200 μm; 200×; scale bar: 50 μm). FTS•B, forsythoside B; APP/PS1, amyloid precursor protein/presenilin 1; 4-HNE, 4-hydroxynonenal; GFAP, glial fibrillary acidic protein; Iba1, ionized calcium-binding adapter molecule 1