Fig. 7

Decreased neuroinflammation in brains of KCa3.1^−/−/APP/PS1 mice. a Levels of activated microglia in CA1 areas of the mouse hippocampus were analyzed by immunostaining of the microglia marker Iba1. b Quantification of activated microglia number/0.01 mm² in the hippocampus (n = 3). Data are presented as the mean ± SEM. *p < 0.05 (one-way ANOVA followed by Dunnett’s post-hoc test). Scale bars: 25 μm. c Levels of reactive astrocytes in the CA1 area of the mouse hippocampus were analyzed by immunostaining of the astrocyte marker GFAP. d Quantification of reactive astrocytes number/0.01 mm² in the hippocampus (n = 3). Data are presented as the mean ± SEM. *p < 0.05 (one-way ANOVA followed by Dunnett’s post-hoc test). Scale bars: 25 μm. e–i Gene deletion of KCa3.1 attenuated expression and release of inflammatory mediators in the brains of KCa3.1^−/−/APP/PS1 mice. e–g Western blots showing protein expressions of COX-2 (e, f) and iNOS (e, g) proteins. f, g Data are presented as the mean ± SEM (n = 3). *p < 0.05, **p < 0.01 (One-way ANOVA followed by the Dunnett’s multiple comparison test). h, i Measurement of TNF-α (h) and IL-1β (i) released by ELISA in homogenated cortex of WT, KCa3.1^−/−, APP/PS1, and KCa3.1^−/−/APP/PS1 mice. Data represent mean ± SEM. *p < 0.05 (one-way ANOVA followed by the Dunnett’s multiple comparison test)