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. 2022 Jul 19;23(14):7933. doi: 10.3390/ijms23147933

Figure 7.

Figure 7

Gβγ-GRK2 inhibition ameliorates synoviocyte inflammation and M1 macrophage differentiation in human cells. Changes in mRNA gene expression of synoviocyte inflammatory markers (A) TNFα and (B) VCAM1 in human synoviocytes (FLS-differentiated SW982 cells and undifferentiated cells (UD)). IL-1β-stimulated SW982 cells were treated with vehicle (IL-1β + V) gallein (1β + G), paroxetine (1β + Px), fluoxetine (1β + Fx), and indomethacin (1β + Indo). Changes in mRNA gene expression of macrophage phenotype markers (C) CD80 and (D) CCL22 in human macrophage cells (M1- and M2-differentiated THP1 cells). Macrophage cells differentiated into M1 or M2 macrophage phenotypes and resting macrophages (M0) were treated with vehicle (M1/M2 + V), gallein (M1/M2 + G), paroxetine (M1/M2 + Px), fluoxetine (M1/M2 + Fx), and indomethacin (M1/M2 + Indo). RT-qPCR from n = 3 experimental replicates. Data are normalized to expression of GAPDH. * p < 0.05 vs. IL-1β + V group; ** p < 0.01 and **** p < 0.0001 vs. M1 + V group; * p < 0.05 and ** p < 0.01 vs. M0 + V group using one-way ANOVA. Values are expressed as means ± SEM.