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Fig. 7 | Journal of Neuroinflammation

Fig. 7

From: β-arrestin1 regulates astrocytic reactivity via Drp1-dependent mitochondrial fission: implications in postoperative delirium

Fig. 7

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

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