Figure 7.
Activation of the NLRP3/HMGB1 pathway partly counteracts the protection against macrophage cuproptosis and cardiomyocyte apoptosis mediated by SLC31A1 knockdown in mice with post-AMI HF. (A) NLRP3 mRNA expression in mouse macrophages determined by RT-qPCR, n = 12; (B) NLRP3, cleaved caspase-1 and ASC protein levels in mouse macrophages measured by western blot, n = 12; (C-E) The Cu2+ level, ATP content, and SDH activity in mouse macrophages assessed by kits, n = 12; (F) Levels of cuproptosis-related proteins FDX1 and DLAT in mouse macrophages determined by western blot, n = 12; (G) Mitochondrial damage in cells assessed by TEM; (H-J) Levels of HMGB1, IL-1β, and TNF-α in mouse serum measured by ELISA, n = 12; (K-L) LVEF and LVEDP detected by echocardiography, n = 12; (M) The NT-proBNP level in mouse serum measured by ELISA, n = 12; (N) Representative images of TTC-stained heart sections and quantification of myocardial infarction, n = 6; (O) Cardiomyocyte apoptosis evaluated by TUNEL staining, n = 6. Data were described as mean ± standard deviation, with multi-group comparisons conducted by one-way ANOVA, followed by Tukey’s post hoc tests. *p < 0.05, **p < 0.01, ***p < 0.001.
