Melatonin regulates Sirt1/Nrf2/GPX4 pathway to inhibit ferroptosis and alleviate myocardial injury caused by sepsis

Figure 1 Melatonin alleviates lipopolysaccharide-induced cardiac dysfunction in vivo. A-D: Echocardiography 24 hours after lipopolysaccharide injection: Left ventricular end-diastolic diameter (A); left ventricular end-systolic diameter (B); ejection fraction (C); and fractional shortening (D); E-H: Serum cardiac injury markers: Brain natriuretic peptide (E); lactate dehydrogenase (F); creatine kinase-MB (G); and cardiac troponin I (F). Data are expressed as mean ± SD; n = 6 mice per group. Group differences were analyzed using one-way analysis of variance with Bonferroni post-hoc testing. ^aP < 0.01 vs control; ^bP < 0.01 vs lipopolysaccharide. BNP: Brain natriuretic peptide; CK-MB: Creatine kinase-MB; cTnI: Cardiac troponin I; EF: Ejection fraction; FS: Fractional shortening; LDH: Lactate dehydrogenase; LPS: Lipopolysaccharide; LPS + Mel: Lipopolysaccharide plus melatonin; LPS + Fer-1: Lipopolysaccharide plus ferrostatin-1; LVEDD: Left ventricular end-diastolic diameter; LVESD: Left ventricular end-systolic diameter.