Fig. 6

Irisin down-regulates p53 to promote the expression of SLC7A11 and consequently inhibits ferroptosis in H9C2 cells. A The effect of the irisin on the time course of p53 degradation in HG-treated H9C2 cells. To inhibit protein synthesis, the cells were treated with 100 μmol/L CHX for the indicated time (n = 4 per group). B Representative fluorescent images of FerroOrange staining in each of the four groups of H9C2 cells (B1) and the quantification (B2) in H9C2 cells (Scale bar = 50 μm; n = 6). C1 Immunoblots of SLC7A11, GPX4, and GAPDH from each of the five groups of H9C2 cells. C2 Quantification of the SLC7A11 and GPX4 bands. All results were normalized to the expression level of GAPDH (n = 4 per group). D Representative Western blotting images (D1) with quantification (D2) from each of the five groups of H9C2 cells showing p53 K382 acetylation andp53 protein levels (n = 4 per group). Data are expressed as the mean ± SD. One-way ANOVA, and Bonferroni’s post-hoc test. ^*P < 0.05, ^**P < 0.01. HG high glucose, p53 tumor suppressor p53, SLC7A11 solute carrier family 7 member 11, and GPX4 glutathione peroxidase 4, CHX cycloheximide, and Ac acetylation