miR-432-5p Inhibits the Ferroptosis in Cardiomyocytes Induced by Hypoxia/Reoxygenation via Activating Nrf2/SLC7A11 Axis by Degrading Keap1

Figure 1

The Fe metabolism is involved in the process of cell hypoxia/reoxygenation (H/R) and ischemia/reperfusion (I/R): (a) the cell morphology (magnification was 100x) and viability of cardiomyocytes under H/R 4 hr and H/R 6 hr decreased compared to normal control by LDH assay, N = 3; (b) H/R leads to increased MDA level, decreased SOD activity, and decreased ratio of GSH/GSSG in cardiomyocytes; (c) representative image of normal heart and I/R heart section stained by H&E (N = 6, magnification was 200x); MI section demonstrates unclear myofibril structure, reticular fibrosis can be seen in myocardium, and lipofuscin can be seen in the cytoplasm of myocardial cells (black arrow); (d) in vivo analysis demonstrated that I/R also caused increased MDA, decreased SOD, and the ratio of GSH/GSSG, N = 6; (e) the immunohistochemistry of 4-HNE in cardiac tissues. I/R induces obviously elevated 4-HNE, one of the products of lipid peroxidation (magnification was 200x); (f) GPX4 and UCP3 protein level decreased after I/R; (g) I/R increased mRNA and protein expression of ferroptosis biomarker PTGS2; the extracellular LDH level decreased under H/R conditions and (h) cell viability (i) had been recovered. , ; N = 6.

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