Fig. 3.

ACSL4 induced pericytes ferroptosis via damaging mitochondria function. (A) Heatmap of differentially metabolites between control groups and LPS treated groups. (n = 6/group) (B) Western blotting analysis of ACSL4 of pericytes after LPS treatment. (C) The relative expression level of ACSL4 after treatment in Si-NC and Si-ACSL4 of pericytes. (D) Cell viability of LPS-stimulated pericytes pre-treated with Si-ACSL4. (E) Cell viability of LPS-stimulated pericytes pre-treated with GSH, Deferoxamine (DFO), Rosiglitazone (Rosi) and Si-ACSL4. (F–H) Confocal images to observe lipid peroxidation (Bar = 25 μm), MitoSOX (Bar = 25 μm) and mitochondria membrane potential (Bar = 10 μm) of LPS-stimulated pericytes after being transfected with Si-ACSL4. (I) Effects of Si-ACSL4 on the mitochondria respiration in pericytes. (J) The relative expression level of PGC-1α after treatment in Si-ACSL4 of pericytes. (K) Transendothelial electrical resistance (TER) of endothelial cells. (L) FITC-BSA leakage in endothelial cells.

For in vitro experiments or cell samples, n = 3 for each group. Data were shown as mean ± SD. ∗∗p < 0.01, ∗∗∗p < 0.001. Statistical significance was determined by one-way ANOVA or two-sided Student's-test as appropriate.