PrA ameliorates ischemia/reperfusion (I/R)‐induced cardiac injury and ferroptosis. A) Schematic diagram of animal experiment process. Time points in the image are representative. B) Serum LDH and C) CK‐MB (fivefold dilution) levels were measured in mice 24 h after sham or I/R surgery, treated with or without PrA (20 mg kg−1 i.g.) (n = 6 per group). D) Evans blue/triphenyltetrazolium chloride (TTC) staining of heart sections in mice 24 h after sham or I/R surgery, treated with or without PrA (20 mg kg−1 i.g.) (scale bars:100 µm). E–I) Representative echocardiographic images from mice 7 d after sham or I/R surgery, treated with or without PrA (20 mg kg−1 i.g.). F–I) Quantitative analysis of LVEF, FS, LVIDd, and LVIDs (n = 6 per group). J) Representative images of Masson's trichrome staining in mice 7 d after sham or I/R surgery, treated with or without PrA (20 mg kg−1 i.g.) (scale bars:1 mm, n = 6 per group). K) Relative mRNA levels of Ptgs2 (n = 6 per group). Quantitative analysis of L) cardiac MDA and (M) serum MDA (n = 6 per group). N) Western blots of cardiac GPX4, ACSL4, and FTH1 (n = 6 per group). O,P) Representative images of Prussian blue iron staining with DAB enhancement (O, scale bar:100 µm) and fluorescent immunohistochemistry staining for DHE (P, scale bar: 20 µm). B,K) Some of the data was normalized. Summary data are presented as the mean ± SEM. Statistical significance was determined using one‐way ANOVA with Tukey's multiple comparisons test. *p < 0.05, **p < 0.01, ***p < 0.001, ****p < 0.0001. Abbreviations: CK‐MB, creatine kinase‐MB; LDH, lactate dehydrogenase; i.g., intragastric; PrA, protosappanin A.