Fig. 3
RA metabolism affected T-cell differentiation to reduce neuroinflammation mediated by the gut-brain axis. (A) The number of FoxP3 + cells in the small intestine of the control group (n = 3). Representative flow cytometry plots of CD4 T cells identified using CD45+ and CD4+ expression. Representative flow cytometry plots of Treg cells (CD45+CD4+FoxP3+) in the small intestine [38] (numbers represent events within the gate as a percentage of CD4+ cells). (B) The number of FoxP3+ cells in the small intestine of the low-dose atorvastatin group (n = 3). (C) The number of FoxP3+ cells in the small intestine of the high-dose atorvastatin group (n = 3). (D) Comparison of the three groups showed that atorvastatin significantly increased the number of FoxP3+ cells (n = 3 per group). (E) Representative flow cytometry analysis of IL-17 production in γδ T cells (CD45+TCR-γδ+) in the small intestine of the control group (n = 3). (F) Representative flow cytometry analysis of IL-17 production in γδ T cells in the small intestine of the low-dose atorvastatin group (n = 3). (G) Representative flow cytometry analysis of IL-17 production in γδ T cells in the small intestine of the high-dose atorvastatin group (n = 3). (H) Quantification of IL-17-producing cells in the small intestine of the three groups. (I) Immunofluorescence of the hippocampus, cerebral cortex, and hypothalamus. Immunofluorescence of neurofibrillary tangles (green) in cerebral tissue. (J and K) The expression of IL-17 in the hippocampus of different groups of rats was detected by western blotting (n = 3 per group). Data are presented as the mean ± SEM. Statistical analyses were performed using one-way ANOVA with Tukey’s multiple comparison test (D, H, J). **P < 0.01, ***P < 0.001, ****P < 0.0001. C: control group, L: low-dose atorvastatin group, H: high-dose atorvastatin group