Fig. 2

PM2.5-induced IL-1β production in oAβ-stimulated microglia is possibly dependent on NLRP3 inflammasome activation. Microglia were stimulated by LPS or oAβ alone for varying time, and the concentration of IL-1β in the culture supernatant was measured by ELISA (a). Microglia primed with LPS for 3 h were washed with fresh serum-free DMEM. LPS-primed microglia were stimulated with oAβ for 12 h and treated with pan-caspase inhibitor Z-VAD-FMK (b) or caspase-1 inhibitor Z-YVAD-FMK (c) for 30 min before PM2.5 exposure. After PM2.5 exposure for 4 h, IL-1β concentration in the culture supernatant was measured by ELISA. All figures are representative of three independent experiments, performed in triplicate. *P < 0.05 vs. LPS-primed microglia stimulated with oAβ. ^#P < 0.05 vs. LPS-primed microglia stimulated with oAβ and PM2.5. d, e LPS-primed microglia were stimulated with oAβ for 12 h and then treated with PM2.5 for 4 h. The protein levels of Caspase-1 p10, pro-caspase-1, and NLRP3 were assessed by western blotting. β-actin was used as loading control. f LPS-primed microglia were stimulated with oAβ for 12 h and then treated with PM2.5 for 4 h. Caspase-1 activity was measured. All figures are representative of three independent experiments, performed in triplicate. *P < 0.05 vs. LPS-primed microglia. ^#P < 0.05 vs. LPS-primed microglia stimulated with oAβ