Fig. 5

β-Arrestin2 mediates the anti-inflammatory effects of Drd2. a Forskolin or dibutyryl cAMP (db-cAMP) failed to abolish the inhibitory effects of quinpirole on the LPS-induced IL-1β production assessed by ELISA in astrocytes. Data are presented as the mean ± S.E.M from four independent experiments, one-way ANOVA, ^**p < 0.01 vs. control group, and ^##p < 0.01 vs. LPS treatment group. b–g Knockdown of β-arrestin2 abolished the anti-inflammatory effects of quinpirole in LPS-treated astrocytes. The astrocytes were transfected with β-arrestin2-specific siRNA (si β-Arr2) for 48 h followed by treated with LPS and quinpirole. b The expression of β-arrestin2 in astrocytes transfected with si β-Arr2 or negative control (NC) for 48 h. Data are presented as the mean ± S.E.M from four independent experiments, t test, ^**p < 0.01 vs. NC group. The levels of IL-1β were determined by qPCR analysis (c) and Elisa analysis (d). Representative immunoblot (e) and quantitative analysis of p-IKK (f) and nuclear p65 (g) in astrocytes. Data are presented as the mean ± S.E.M from four independent experiments, two-way ANOVA, ^*p < 0.05 vs. control group, ^#p < 0.05 vs. LPS treatment group, and ^$p < 0.05 vs. LPS + quinpirole group