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

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Copyright © 2021 Dai, Ye, Zhong, Chen, Hong, Zhao, Su and Lu.

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

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GSDMD silencing alleviated myocardial cell injury induced by LPS. (A and E) CCK-8 assay was applied to measure cell viability of each group. (B and F) LDH release in supernatants of each group. (C and G) The level of IL-1β in supernatants of each group. (D and H) Expressions of GSDMD and GSDMD-NT protein in H9c2 cells and primary cardiomyocytes were measured by Western blotting analysis. The results were normalized to the expression of GAPDH. The data are expressed as the mean ± SD (n = 3). (I) After transfected with siRNA of Gsdmd, H9c2 cells were treated with LPS plus nigericin to establish the myocardial injury model. Expressions of GSDMD and GSDMD-NT protein in H9c2 cells were measured by Western blotting analysis (n = 3). (J) CCK-8 assay was applied to measure cell viability of each group. (K) LDH release in supernatants of each group. The data are expressed as the mean ± SD (n = 3). **p < 0.01, ***p < 0.001.