Xanthohumol Protects the Rat Myocardium against Ischemia/Reperfusion Injury-Induced Ferroptosis

Figure 4

The mechanism of XN inhibited lipid peroxidation. (a) Representative fluorescence images of intracellular ROS using CM-H₂DCFDA in neonatal cardiomyocytes. Treatment with Fe-SP (2 μM) significantly increased the level of intracellular ROS (green, central panel), and this effect was abolished by XN (50 μM) (right panel). Hoechst 33342 was used to identify the cell nuclei. Scale bars: 100 μm. (b) Representative fluorescence images of lipid peroxidation using C11 BODIPY 581/591 in neonatal cardiomyocytes. Treatment with Fe-SP (2 μM) significantly increased the level of lipid peroxidation (green, central panel), and this effect was abolished by XN (50 μM) (right panel). Scale bars: 100 μm. (c) Treatment with XN significantly inhibited Fe-SP-increased the level of ACSL4 protein (). (d) Treatment with XN increased the level of GPX4 protein as compared with the Fe-SP-treated group (). (e) Treatment with XN did not significantly affect the Fe-SP-reduced the level of FTH protein (). (f) Treatment with XN significantly inhibited the Fe-SP-increased level of NRF2 protein (). All data represent . , versus the control group; ^#, versus the Fe-SP. Con: control; Hoe: Hoechst 33342.

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