Inhibition of NLRP3 inflammasome activation on the inflammatory response of macrophage induced by silica dust

Objective: To investigate the effect of inhibiting the activation of NLRP3 inflammatory bodies on the inflammatory response of macrophages induced by silica (SiO(2)) dust. Methods: Rat alveolar macrophages (NR8383) cells were used to establish the cell model, which was divided into four groups: blank control group, dust exposure group (50 mg/L silica dust suspension) , NLRP3 inhibitor group (50 mg/L silica dust suspension and 20 μmol/L NLRP3 inhibitor) , luteolin group (50 mg/L silica dust suspension and 20 μmol/L luteolin) . Samples were collected at 12, 24 and 48 hours after culture. The secretion of inflammatory factors IL and TGF-β(1) were detected by ELISA. The levels of NLRP3 and Caspase-1 were detected by Western Blot. Results: Compared with the blank control group, the survival rates of NR8383 cells in the dust exposure group, NLRP3 inhibitor group and luteolin group were all decreased after 12, 24 and 48 hours of dust exposure, and the expression levels of IL-1β, IL-18, TGF-β1, NLRP3 and Caspase-1 were significantly increased (P<0.05) . Compared with the dust exposure group, NR8383 cells in NLRP3 inhibitor group and luteolin group had higher cell survival rates and lower levels of IL-1β, IL-18, TGF-β1, NLRP3 and Caspase-1 after 12, 24 and 48 hours of dust exposure (P<0.05) . Compared with the NLRP3 inhibitor group, the IL-1β level of NR8383 cells in luteolin group decreased significantly at 12, 24 and 48 h, the IL-18 and TGF-β1 levels decreased significantly at 48 h, the NLRP3 and Caspase-1 levels decreased significantly at 24 h (P<0.05) . Conclusion: Inhibition of NLRP3 inflammaasome activation can reduce the inflammatory response of macrophages induced by SiO(2) dust.