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. 2020 Sep 22;123(12):1737–1748. doi: 10.1038/s41416-020-01088-w

Fig. 1. Differentiation of CB-11-treated 3T3-L1 cells into adipocyte-like cells.

Fig. 1

a The chemical structures and molecular formulas of CB11. b CB11(30 μΜ)-, Ciglitazone (Cig, 10 μΜ)-, or CB11 (30 μΜ) + GW9662 (20 μM)-mediated adipocyte differentiation was assessed by the presence of Oil Red O-stained droplets. Oil Red O-stained cells were detected using a light microscope by scoring cells from each dish at ×400 magnification. c 3T3-L1 cells were transiently transfected with 2 μg of the PPAR response element reporter gene (pGL3-ppre vector) and treated with CB11 or Cig at the doses indicated (CB11, 10 or 30 μΜ; Cig, 10 μΜ); *p < 0.05. d Western blot analysis of PPARɣ analysed at the indicated doses in CB11 or Cig-treated 3T3-L1 cells. β-actin was used as a protein loading control. e Effect of GW9662 (20 μM) on CB11 (30 μΜ) -treated 3T3-L1 cells. 3T3-L1 cells were pre-treated with GW9662 (20 μΜ) for 4 h and then treated with CB11 for 24 h (30 μΜ). 3T3-L1 cells were also treated with Cig (10 μΜ) as a control. Total lysates were interrogated by Western blot analysis to identify inhibition of PPARɣ. β-actin was used as a protein loading control.