Fig 1: Overexpression of Hmox1 counteracted the effect of SMY on ferroptosis. (A) The heart/body weight ratio was calculated. (B, C) Cardiac mitochondria and cytosolic nonheme iron (B) and serum nonheme iron (C) were detected by an iron assay kit (#ab83366, Abcam) in mice treated with DOX with or without SMY or Hmox1-OE. (D, E) Western blot analysis of Hmox1 and GAPDH protein levels in control mice, AAV-control mice, and AAC-Hmox1 mice. (F–J) Western blot analysis of FTH1, TFR1, GPX4, and Hmox1 protein contents. The results were presented as mean ± SEM. *means compared with the other group, P < 0.05, **means compared with the other group, P < 0.01.
Fig 2: SMY inhibited iron overload, lipid peroxidation, and serum enzymology. (A, B) Serum (A), cardiac mitochondrial, and cytosolic (B) nonheme iron were detected by an iron assay kit (#ab83366, Abcam). (C, D) Serum (C) and cardiac (D) MDA contents were measured by lipid peroxidation MDA assay kit (Beyotime, S0131S) in control mice and mice treated with DOX with or without SMY or mitoTEMPO. (E, F) Serum LDH (E) and CK-MB (F) levels were examined by commercial assay kits (Beyotime, C0016 and ZCIBIO, ZC-38269) according to the manufacturer’s instructions. The results were presented as mean ± SEM. ##means compared with control group, P < 0.01; *means compared with DOX group, P < 0.05, **means compared with DOX group, P < 0.01.
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