FIGURE 2.

Ferroptosis inhibition attenuated myocardial injury and inflammation following CME. (A,B) The expression levels of Gpx4 and Ptgs2 mRNA (n = 6). (C–F) Western blotting showing the expression of Gpx4, Slc7a11, and Ptgs2 (n = 4). (G–I) Levels of GSH, Fe²⁺, and MDA in myocardial tissues (n = 6). (J,K) RT-qPCR was performed to quantify levels of IL-1β and TNF-α (n = 6). (L–N) Western blotting showing the expression of IL-1β and TNF-α (n = 4). (O) Serum levels of cTnT were decreased in the DFO group (n = 6). (P–R) Cardiac LVEF and FS detected by echocardiography (n = 10). GAPDH served as an internal control and was performed to quantitatively normalized the protein data. Data are presented as the normalized mean ± SEM (to Saline) or mean ± SEM. Values in salines were averaged and normalized to 1 (A–O). *p < 0.05. **p < 0.01. CME: coronary microembolization; DFO: deferoxamine; LVEF: left ventricular ejection fraction; FS: fractional shortening; cTnT: cardiac troponin T; Gpx4: glutathione peroxidase 4; Slc7a11: solute carrier family 7 member 11; Ptgs2: prostaglandin-endoperoxide synthase-2; MDA: malondialdehyde; GSH: glutathione; IL-1β: interleukin 1 beta; TNF-α: tumor necrosis factor alpha.