Fig. 5: Stimulation of branched-chain amino acid catabolism can blunt ferroptosis.

a (Top) Strategy for injecting intraperitoneally BT2 while induing CKD with cisplatin in mice. (Bottom) RT-qPCR analysis showing the transcript levels of selected genes involved in inflammation, apoptosis, ferroptosis, cell cycle arrest, and fibrosis. Each dot indicates individual, biologically independent mice (n = 5 per group). Data were normalized to their respective control and presented as Mean ± SEM. n.s., not significant (p > 0.05), unpaired, two-sided t-test. b Immunofluorescence microscopy showing Acsl4 (Top) and 4-HNE (Bottom) expression in the cisplatin-injured kidney in the presence or absence of BT2 with Lotus tetragolonobus lectin (LTL) and LRP2 as kidney proximal tubule markers and DAPI as a nucleus marker. c Quantification of Acsl4 protein expression in BUMPT cells of the mouse kidney proximal tubule origin from three independent experiments. Each dot represents biologically independent samples (n = 3 per group). Data were normalized to their respective control and presented as Mean ± SEM. n.s., not significant (p > 0.05), unpaired, two-sided t-test. d Alamar Blue assay to measure cell survival of ferroptotic cell death. Each dot represents biologically independent samples (n = 6 per group). Data were normalized to their respective control and presented as Mean ± SEM. Statistical significance was determined using a two-way RM ANOVA test. Source data are provided as a Source Data file.