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. 2023 Jan 3;11(1):449–463. doi: 10.1016/j.gendis.2022.12.003

Figure 3.

Fig. 3

CD36 deficiency was resistant to ferroptosis. (A) Representative transmission electron microscopy images. Mitochondrial outer membrane rupture or mitochondrial crest injury are indicated by red arrows. (B) Quantification of ferroptosis biomarker ACSL4, xCT, and GPX4 mRNA levels by qPCR (n = 3). (C) Western blotting was used to detect the expression of ferroptosis biomarkers ACSL4, xCT, and GPX4 in kidney tissues of four mouse groups (n = 3). Data are expressed as means ± standard deviation (SD). ∗P < 0.05 and ∗∗P < 0.01 vs. control group. (D) After CD36 overexpression or silencing and treatment with normal saline and cisplatin, western blotting was used to detect the expression of CD36 and ferroptosis biomarkers ACSL4, xCT, and GPX4 in TCMK-1 cells; quantitative statistical analysis for each protein (n = 3) was also performed. (E, F) MDA and GSH levels in mice (n = 8). (G) Change in ROS generation in TCMK-1 cells. ROS levels were determined by flow cytometry. (H) Mean ROS fluorescence intensity was expressed as mean ± SD of three independent measurements. ∗P < 0.05 vs. the indicated sample (n = 3).