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. 2026 Feb 23;17:1707203. doi: 10.3389/fimmu.2026.1707203

Figure 2.

Graphs and images illustrate experimental data comparing different groups: Sham, AMI, AMI+sh-NC, and AMI+sh-SLC31A1. Charts A to C show levels of Cu²⁺, ATP, and SDH. Chart D includes protein expression of FDX1 and DLAT, with Western blot images. Chart E displays mitochondrial damage with corresponding images. Charts F to H show HMGB1, IL-1β, and TNF-α levels. Significant differences are indicated with asterisks.

SLC31A1 knockdown arrests cuproptosis and HMGB1 release by regulating copper metabolism imbalance, alleviating inflammatory responses in macrophages of mice with HF after AMI. (A-C) Cu2+ level, ATP content and SDH activity in mouse macrophages determined by kits; (D) Levels of cuproptosis-related proteins FDX1 and DLAT in mouse macrophages measured by western blot; (E) Mitochondrial damage in cells detected by TEM; Levels of HMGB1 (F), IL-1β (G), and TNF-α (H) in mouse serum measured by ELISA. n = 12. 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.