Fig. 2

PPARγ agonists induce CD36/CPT1-mediated FAO during Treg differentiation. The naïve CD4⁺ T cells were prepared and treated with anti-CD3/CD28 in the presence or absence of TGF-β, rosiglitazone (10, 30 μM), 15d-PGJ2 (3, 10 μM) as well as morin (10, 30 μM) for 48 h. a The fatty acid uptake was examined by flow cytometry using BODIPY-C16. b The OCR was monitored by Seahorse XFe 96 analyzer. c The mitochondrial mass was observed with a fluorescence microscope using MitoTracker Green. d The mitochondrial membrane potential was analyzed by flow cytometry using a JC-1 assay kit. e The level of acetyl-CoA was determined using a commercial acetyl-CoA assay kit. f–k The mRNA expression levels of CD36, CPT1, ACADL, ACADM, HADHA as well as HADHB were measured by Q-PCR. l The protein levels of CD36 and CPT1 were detected by western blotting. Data were presented as the means ± S.E.M. of three independent experiments (n = 3). ^#P < 0.05, ^##P < 0.01 versus control group; *P < 0.05, **P < 0.01 versus TGF-β group (model group)