Fig. 8: Nicotine altered gene Expression of the aged mice brain and promoted neurogenesis and inhibited inflammation.

a Volcano plots of differentially expressed genes (n = 3, biologically independent samples/group). b The Gene KEGG pathways related to “Signal transduction”, “Ageing”, “Immune system”, “Transcription” between control mice and nicotine mice after nicotine administrated for 6 months (n = 3, biologically independent samples/group). c Heatmap depicting transcriptional profiles of KDA gene and Go function enrichment (n = 3, biologically independent samples/group). d The “GO_biological processes” were related to neurogenesis: nervous system development, neuron differentiation, brain development, dentate gyrus development, central nervous system neuron development (n =3,  biologically independent samples/group). e Representative microscopic fields and quantification of Dcx-positive cells in the dentate gyrus (DG) of the hippocampus of naïve aged mice administered with or without nicotine (n = 3, biologically independent samples/group arrowheads point to individual cells; scale bar, 100 μm). Dapi, 4′, 6-diamidino-2-phenylindole. f Western blot and quantification of the protein expression of BDNF, Doublecortin in the hippocampus of aged mice administered with or without Nicotine (n = 3 biologically independent samples/group). Quantification is normalized to GAPDH. g Heatmap depicting transcriptional profiles of creb1 and Atf2 in aged mice brain after nicotine administration (n = 3, biologically independent samples/group). h Western blot and quantification of the protein expression of JAK2 and STAT3 in the cortex and hippocampus: phosphorylate-JAK2/JAK2 ratio and phosphorylate-STAT3/STAT3 ratio of aged mice administered with or without nicotine (n = 3, biologically independent samples/group). Quantification is normalized to GAPDH. Data are means ± SEM. p values were determined by two-sided Student’s t test (e–g), or two-way ANOVA analysis and Fisher’s least significant difference (h).