Fig. 6: NaB modulates the function of neurons by modulating Cxcl16 expression in astrocytes via epigenetic modification of H3K27bz.
(A) Volcano plot of 1013 DEGs between PBS- and NaB-treated primary astrocytes. Red dots represent 665 upregulated DEGs, blue dots represent 348 downregulated DEGs, n = 4 biological replicates /group. (B) Cxcl16 expression in different NaB-treated groups was analyzed by real-time PCR. n = 3 biological replicates /group. (C) Western blotting analysis of Histone Kbz and H3 expression in primary astrocytes treated with or without NaB, n = 3 biological replicates /group. (D) Western blotting analysis of H3K27bz and H3 expression in primary astrocytes treated with or without NaB. n = 3 biological replicates /group. (E) The distribution of the significantly increased peak according to CUT & Tag analysis for H3K27bz in primary astrocytes treated with or without NaB, n = 4-5 biological replicates /group. (F) NFR peak distribution of the significantly induced peaks of H3K27bz binding in primary astrocytes treated with or without NaB, n = 5 biological replicates /group. (G) Genomic binding patterns of H3K27bz and ATAC-seq at the genomic loci of Cxcl16 in primary astrocytes. (H) Schematic diagram of the impairment and epigenetic mechanism of Lactobacillus plantarum and its derived metabolite sodium benzoate. Data were presented as mean ± SEM, and statistical significance was determined by Unpaired t test (C and D), Tukey’s multiple comparisons test (B), significant differences were classified as follows: ns p > 0.05, *p < 0.05, ***p < 0.001, ****p < 0.0001.
