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Fig. 3 | Journal of Neuroinflammation

Fig. 3

From: β-Arrestin2-biased Drd2 agonist UNC9995 alleviates astrocyte inflammatory injury via interaction between β-arrestin2 and STAT3 in mouse model of depression

Fig. 3

Drd2-biased β-arrestin2 pathway was involved in the loss of astrocytes. A Concentrations of DA, DOPAC, 5-HT, 5-HIAA, HE, and HVA in the brain were detected by HPLC. (Control group: n = 8; CUMS group: n = 10). B mRNA levels of the dopamine receptor family (Drd1, Drd2, Drd3, Drd4, and Drd5) in the hippocampus were detected by qRT-PCR. (Control group: n = 12; Susceptible group: n = 12). C Protein level of Drd1, Drd2, β-arrb2, β-arrb2 and GFAP were detected in the control, susceptible, and resilient mice groups. D Colocalization of GFAP (the marker of astrocytes) with β-arrestin2 and colocalization of IBA-1 (the marker of microglia) with β-arrestin2 by immunofluorescent staining in the hippocampus of Control and CSDS groups. Red, GFAP; Pink, IBA-1; Green, β-arrestin2; Blue, DAPI. Scale bar, 100 μm. Arrow: GFAP+ astrocytes co-localize with β-arrestin2 in the hippocampus. E Immunofluorescence of GFAP in the hippocampus of WT and Arrb2−/− CUMS mouse model. Red, GFAP; Blue, Hoechst. Scale bar, 100 μm. F Counting GFAP+ astrocytes in the hippocampus of WT and Arrb2−/− CUMS mouse models. G Levels of cytokines such as TNF-α, IL-6, and IL-1β were detected by RT-PCR in the hippocampus of WT and CUMS mouse models (n = 6). Corticosterone (H) and levels of cytokines (I) such as IL-1β, IL-6, and TNF-α were detected by ELISA in the WT and CUMS mouse model plasma (H n = 6; I n = 3). A, B Bars and error flags represent the means ± SEM statistically significant by Student t test; ns, P > 0.05, *P < 0.05, **P < 0.01. F, I Data are analyzed using two-way ANOVA, then combined with Tukey to assess the differences between groups. *P < 0.05, **P < 0.01, ***P < 0.001 VS WT Control group. $P < 0.05, $$P < 0.01, $$$P < 0.001

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