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. 2021 Apr 12;17(7):1693–1707. doi: 10.7150/ijbs.54604

Figure 3.

Figure 3

BBR inhibited lipogenesis, fatty acid uptake and fatty acid oxidation of liver tissues. (A-C) The protein levels of representative key-enzymes in lipid pathways of liver tissues, such as SCD1 and FADS1 for lipogenesis (A), FABP1 and CD36 for fatty acid uptake (B), as well as CPT1A and ACADL for fatty acid oxidation (C). Relative signal strength was quantified for each band (n = 3). (D-F) Mouse liver mitochondria of carnitine + palmitoyl CoA dependent OCR indicating CPT1+2 activities (D), palmitoyl carnitine dependent OCR indicating CPT2 activity (E), and β-ketothiolase activity indicating β-oxidation activity (F) (n = 6). (G) Fatty acid consumption in the primary hepatocytes after the cells were incubated with blank, OA, OA+BBR and OA+ROT for 24 h (n = 4). Data were expressed as means ± SEM. *P < 0.05.