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. 2022 Jul 6;13(7):583. doi: 10.1038/s41419-022-05047-6

Fig. 7. Pol β deficiency exacerbates macrophages pyroptosis via the cGAS/STING/NF-κB pathway in vitro and in vivo.

Fig. 7

A, B RAW264.7 cells were pretreated with 10 μM CCCP or 10 μM JSH-23 for 2 h, treated with 1 μg/mL LPS for 4 h, and then treated with 5 mM ATP for the final hour. The protein levels were examined by Western blotting. Data are representative blot of three independent experiments. C Representative images of NF-κB p65 staining. Scale bar, 10 μm. Lower panel: statistical analysis, the data represent the mean ± SEM from more than 100 cells for each group; *P < 0.05, **P < 0.01, ***P < 0.001, one-way ANOVA. The levels of IL-1β (D) and IL-18 (E) secreted by macrophages were analyzed by ELISA. Data present the mean ± SEM of three independent experiments, *P < 0.05, **P < 0.01, ***P < 0.001, one-way ANOVA. The protein levels in the ankles of Pol β knockdown-CIA mice (F) and Pol β R137Q-CIA mice (G). Data are representative blot of three independent experiments. H Representative immunofluorescence images showing NF-κB p65 phosphorylation in macrophages in the ankles of CIA mice. Scale bar, 500 μm. J Schematic diagram showing our proposed mechanisms of Pol β deficiency exacerbating macrophage pyroptosis through activating the cGAS-STING-NF-κB pathway.