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. 2022 Feb 12;12(9):3650–3666. doi: 10.1016/j.apsb.2022.02.003

Figure 1.

Figure 1

Ferroptosis is triggered in liver tissue of MAFLD patients. (A) Representative H&E histological analysis showing the MAFLD pathology in liver tissue from individuals with or without MAFLD (n > 4 images per individual). Scale bar, 100 μm. (B) The levels of MDA, total-SOD and total-TAC in liver from individuals with or without MAFLD. (C) Immunohistochemistry analysis of 3-nitrotyrosine in liver from individuals with or without MAFLD. Scale bar, 100 μm. (D, E) Immunoblotting (D) and immunohistochemistry analysis (E) of 4-HNE-protein adducts in liver from individuals with or without MAFLD. Quantitative analyses were performed. Scale bar, 100 μm. (F) The mRNA level of NOX1 and NOX4 in liver from individuals with or without MAFLD. (G) The mRNA level of transferrin, FTH and FTL in liver from individuals with or without MAFLD. (H) Immunoblotting analysis of ferritin and transferrin in liver from individuals with or without MAFLD. Transferrin dimer was also detected by the antibody against transferrin in immunoblotting. Tubulin was used as a loading control in immunoblotting. (I) Relative mRNA levels of GPX4 isoform A and C in liver tissue from human with or without MAFLD. (J) Detection of GPX4 isoform A and GPX4 isoform C in liver tissues from human with or without MAFLD. Data are presented as mean ± SEM and analyzed by unpaired t-test, n = 7 per group; ∗P < 0.05, ∗∗P < 0.01, ∗∗∗P < 0.001 vs. Control.