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Fig. 1 | Journal of Neuroinflammation

Fig. 1

From: Fluoxetine inhibited the activation of A1 reactive astrocyte in a mouse model of major depressive disorder through astrocytic 5-HT2BR/β-arrestin2 pathway

Fig. 1

CMS-induced depressive-like behaviors, loss of astrocyte and A1 astrocyte reactivity are rescued by fluoxetine administration. C57BL/6 J mice were subjected to CMS for 6 weeks and then intraperitoneal injected with a vehicle (Control, 0.9% saline) or fluoxetine (10 mg/kg/day) for another 4 weeks. A Sucrose preference percentage during 10 weeks. B, C Immobility time of mice in TST (B) and FST (C). D, E Immunofluorescence staining (D) and area (E) of GFAP+ astrocyte in the hippocampus. F, G Immunohistochemical staining (F) and total branch number (G) of GFAP+ astrocyte in the hippocampus. H Heatmap of A1-special and A2-special transcripts in the hippocampus as analyzed by RT-qPCR. I, J Protein levels of C3 in the hippocampus. KN Proportion of C3 (K, L) and Serping1 (M, N) in astrocyte in the hippocampus. Scar bar, 20 μm in D, K, M; Scar bar, 40 μm in F. Quantitative data are mean ± s.e. Data were analyzed using two-way ANOVA, then combined with Tukey’s multiple comparison to assess the differences between groups. A, B: n = 8 per group; C: n = 9 CON with saline and CMS with FLX, n = 8 CMS with saline and CON with FLX; DN n = 4 per group; biologically independent animals. A, H: **P < 0.01, and ***P < 0.001 vs respective Control mice treated with saline; #P < 0.05, and ###P < 0.001 vs CMS mice treated with saline. BG, J, L, N: *P < 0.05, **P < 0.01, and ***P < 0.001

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