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

Figure 1

XN protects H9c2 cardiomyoblasts against ferroptotic cell death. Treatment with (a) Fe-SP (0.5 μM) or (b) RSL3 (0.1 μM) for 16 h decreased the viability of H9c2 cardiomyoblasts detected using the MTT assay, and this effect was inhibited by cotreatment with XN (5-20 μM) or a ferroptosis inhibitor (ferrostatin-1, Fer-1, 1 μM or liproxstatin-1, Lip-1, 2 μM) (). Confocal images of H9c2 cardiomyoblasts treated with (c) Fe-SP (0.5 μM) or (d) RSL3 (0.1 μM) for 16 h were measured using Hoechst 33342 and lipid ROS probe C11 BODIPY 581/591. A significant increase of the lipid peroxidation was observed (green), and this effect was abolished by XN (10 or 20 μM), Fer-1 (1 μM), or Lip-1 (2 μM). Fe-SP (0.5 μM) or RSL3 (0.1 μM) reduced H9c2 cardiomyoblasts number, but did not induce chromatin condensation. . (e) Treatment with Fe-SP or RSL3 for 16 h enhanced the malondialdehyde content in H9c2 cardiomyoblasts detected using the TBARS assay, and this effect was inhibited by cotreatment with XN (10 or 20 μM) (). (f) XN (10 or 20 μM) significantly decreased the levels of Ptgs2 mRNA in H9c2 cardiomyoblasts-treated with Fe-SP or RSL3 for 16 h, was measured using real-time PCR (). All data represent . , versus the control group; ^#, versus the Fe-SP; ^$, versus the RSL3. Con: control; Veh: vehicle; Hoe: Hoechst 33342.

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