Figure 5.

DSC inhibits the activation of NLRP3 inflammasome in vivo and in vitro. A, Colitis was induced as described in Materials and Methods and treated with or without DSC (50 mg/kg). Representative bands and quantitative analyses of NLRP3, caspase‐1 p20, cleaved IL‐1β and cleaved IL‐18 in colonic tissues. The β‐actin was used as loading control (n = 8 in each group). B, Colitis was induced as described in Materials and Methods and treated with or without lentiviral Nox4 shRNA. Representative bands and quantitative analyses of NLRP3, caspase‐1 p20, cleaved IL‐1β and cleaved IL‐18 in colonic tissues. The β‐actin was used as loading control (n = 8 in each group). C, NLRP3 inflammasome was induced in BMDM as described in Materials and Methods and treated with DSC (50 μmol/L). Representative bands of NLRP3, ASC and caspase‐1 in BMDM and caspase‐1 p20 in supernatant (SN) by Western blot and quantitative analyses of IL‐1β in supernatant by ELISA. The β‐actin was used as loading control. Data shown are means ± SEM of n = 8 in each group. *P < 0.05 vs Control cell or mice (CTL), ^#P < 0.05 vs DSS‐treated mice or LPS + nigericin‐stimulated cells