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. 2021 Nov 8;9:779432. doi: 10.3389/fcell.2021.779432

FIGURE 5.

FIGURE 5

GSDMD regulated NLRP3 inflammasome activation in septic myocardial dysfunction induced by LPS. (A,B) Heat map and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analyses of the transcriptome of heart tissues from WT and Gsdmd −/− (n = 3) mice treated with LPS. (C) Expressions of NLRP3 and caspase-1 protein in H9c2 cells were measured by Western blotting analysis. The results were normalized to the expression of GAPDH. (D) H9c2 cells were pretreated with NLRP3 inhibitor or caspase-1 inhibitor for 1 h and subsequently stimulated with LPS plus nigericin. CCK-8 assay was applied to measure cell viability of each group (n = 4). (E) The LDH release in supernatants of each group (n = 3). (F) The level of IL-1β in supernatants of each group (n = 3). (G) Expressions of NLRP3 and caspase-1 protein in heart tissue were measured by Western blotting analysis. The results were normalized to the expression of GAPDH (n = 6). (H) After transfected with siRNA of Gsdmd, H9c2 cells were treated with LPS and nigericin to establish the myocardial injury model. Expressions of NLRP3, caspase-1, and P65 protein in H9c2 cells were measured by Western blotting analysis. The results were normalized to the expression of GAPDH (n = 3). (I) The level of IL-1β in supernatants of each group (n = 3). The data are expressed as the mean ± SD. *p < 0.05, **p < 0.01, ***p < 0.001.