Fig. 3

Famotidine triggered NLRP3 inflammasomes form. A BGC823 and (B) AGS cells were treated with or without famotidine for 72 h, mRNA levels of indicated inflammasome-related genes were analyzed by RT-qPCR. Data represented the mean ± s.d. of three independent experiments and were analyzed by t test for significance versus Control group (0 μm), ***P < 0.001, **P < 0.01, *P < 0.05 versus control group(0 μm). C BGC823 and AGS cells were treated as indicated and at 72 h post-treatment, cells were harvested to extract total proteins. The SDS-PAGE and immunoblotting were performed to detect indicated proteins, and relative protein expression were quantified and analyzed by t test. Data represented the mean ± s.d. of three independent experiments and were analyzed by t test for significance versus Control group (0 μm), ***P < 0.001, **P < 0.01, *P < 0.05 versus control group(0 μm). the gels/blots and quantitative were processed in parallel. D BGC823 and AGS cells were left untreated or treated with Caspase-1 inhibitor VX-765 for 1 h, followed by famotidine stimulation for another 71 h, the content of IL-18 level in indicated group were measured by IL-18 Elisa kit assay. Data represented the mean ± s.d. of three independent experiments and were analyzed by two-way ANOVA with multiple comparisons, followed by Bonferroni post hoc test for significance. ***P < 0.001, **P < 0.01. E the total protein was collected from above group in D, whole cell lysates were separated by SDS-PAGE and assayed with the antibodies against the indicated proteins. β-actin was determined to ensure equal loading. The quantified result was analyzed by two-way ANOVA with multiple comparisons, followed by Bonferroni post hoc test for significance. ***P < 0.001, **P < 0.01