Fig. 4

Genetic disruption of TRPA1 channel function increases astrogliosis but decreases inflammation in hippocampus of APP/PS1 Tg mice. (a) Immunostaining of hippocampus specimens from 8-month-old WT, TRPA1^−/−, APP/PS1 Tg and APP/PS1 Tg/TRPA1^−/− mice with anti-GFAP antibody, then Texas red-conjugated secondary antibody. (b) Western blot analysis of protein levels of GFAP and α-tubulin. ELISA of (c-f) IL-1β, IL-6, IL-4 and IL-10 secretion and (g, h) NF-κB and NFAT DNA binding activity in brain specimens from 8-month-old WT, TRPA1^−/−, APP/PS1 Tg and APP/PS1 Tg/TRPA1^−/− mice. (i) Immunostaining of hippocampus specimens from 8-month-old APP/PS1 Tg and APP/PS1 Tg/TRPA1^−/− mice with the antibodies anti-GFAP, anti-IL-1β, IL-6, IL-4 or IL-10, then FITC- or Texas red-conjugated secondary antibody. Bar = 50 μm. GFAP-positive cells (red color) denote astrocytes; IL-1β-, IL-6-, IL-4- and IL-10-positive astrocytes (green color) are indicated by arrowheads, arrows, stars or dots, respectively. Data are mean ± SEM from 8 mice in each group. *, P < 0.05 vs. WT mice. #, P < 0.05 vs. APP/PS1 Tg mice