Fig. 5

Asperosaponin VI induces an anti-inflammatory microglial phenotype via PPAR-γ. A Timeline of the experimental process on the effect of GW9662 on ASA VI-treated CMS mice. B Effects of GW9662 treatment on levels of p-PPAR-γ, PPAR-γ-1, and PPAR-γ-2 in hippocampus of ASA VI + CMS mice (n = 3, each sample in triplicate). C and D Effects of GW9662 treatment on microglia with pro- or anti-inflammatory phenotypes in hippocampus of ASA VI + CMS mice. Scale bar, 50 μm. E Effects of GW9662 treatment on the ratio of Arg-1⁺ microglia to iNOS⁺ microglia in hippocampus of ASA VI + CMS mice. F Effects of GW9662 treatment on mRNA levels of pro-inflammatory cytokines (TNF-α, IL-1β, and IL-6), anti-inflammatory cytokines (IL-10 and TGF-β) and BDNF. G Effects of GW9662 treatment on protein levels of IL-1β and IL-10 in hippocampus of ASA VI + CMS mice. Data for individual animals are displayed (mean ± SEM, n = 3–6), B–E and G *p < 0.05, **p < 0.01, ***p < 0.001 (one-way ANOVA with Tukey’s multiple-comparisons test). F *p < 0.05, **p < 0.01, ***p < 0.001 vs. Ctrl group, ^#p < 0.05, ^##p < 0.01 vs. CMS group, ^&p < 0.05, ^&&p < 0.01, ^&&&p < 0.001 vs. CMS + ASA VI group (one-way ANOVA with Tukey’s multiple-comparisons test)