Fig. 4

β-arrestin1 deletion aggravates the neurotoxic reactivity of primary astrocytes. A Schematic of the experimental design. B Expression of C3, Serping1 and Psmb8 in the primary astrocytes. C Densitometric analysis of C3, Serping1 and Psmb8. D Heat map of A1 astrocytic genes in primary cell cultures. E Immunofluorescent staining of C3 (green) and GFAP (red) in primary astrocytes. F Immunofluorescent staining of Serping1 (red) and GFAP (green) in primary astrocytes. G Relative co-localized signals of the GFAP-positive and C3-positive immunofluorescent particles between groups. H Relative co-localized signals of the GFAP-positive and Serping1-positive immunofluorescent particles between groups. I Astrocytes were stained with MitoSOX and analyzed by flow cytometry. J JC-1 staining in astrocytes were analyzed by flow cytometry. K Quantification of the mitochondrial ROS in MitoSOX staining. L Quantification of the loss of mitochondrial membrane potential in JC-1 staining measured by flow cytometry. M Oxygen consumption rates were evaluated by Seahorse. N Quantification of oxygen consumption for ATP production, basal respiration and proton leak. O ATP levels in astrocytes. Data were analyzed by two-way ANOVA followed by Tukey's multiple comparisons test. ^*P < 0.05, ^**P < 0.01 and ^***P < 0.001 vs. the WT CON-MCM group. ^#P < 0.05, ^##P < 0.01 and ^###P < 0.001 vs. the WT LPS-MCM group. Values are presented as means ± SEM from at least three independent experiments