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Fig. 4 | Microbiome

Fig. 4

From: Depletion of acetate-producing bacteria from the gut microbiota facilitates cognitive impairment through the gut-brain neural mechanism in diabetic mice

Fig. 4

Exogenous acetate supplement increases hippocampal synaptophysin level in mice with gut microbiota dysbiosis induced by vancomycin. The changes in the mRNA expression levels of a Arc, b c-Fos, c EGR, and d SYP in normal control (CON), type 1 diabetic (T1D), and vancomycin-treated T1D (T1DV) mice at 3, 7, and 11 weeks. e Correlation network analysis among acetate, cognitive parameters, and synaptic plasticity-related genes. The relationship was analyzed by Pearson’s correlation and red line represents positive correlation. f Relative SYP mRNA expression level in the hippocampus of CON, T1D, T1DV, and T1DV treated with acetate (T1DVA) mice at 7 weeks. g, h The level of SYP protein detected by Western blotting and the corresponding quantitative data in the hippocampus of CON, T1D, T1DV, and T1DVA mice at 7 weeks (n=3 mice per group). i, j Representative SYP immunostaining and the quantified relative SYP intensity in hippocampal CA1 region of CON, T1D, T1DV, and T1DVA mice at 7 weeks (n=3 mice per group). Scale bar = 400 μm. k, l The change in the relative SYP mRNA expression level between CON and vancomycin-treated CON (CONV) mice at 3, 7, and 11 weeks and between CON and CONV treated with acetate (CONVA) mice at 11 weeks. Data are presented as mean±s.d. of n=5–6 mice per group. The difference between two groups was determined by two-tailed unpaired Student’s t test with Bonferroni correction. The differences among three or four groups were analyzed by one-way ANOVA with Bonferroni’s multiple comparisons test, and data with different lowercase codes are significantly different (P < 0.05)

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