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. 2013 Mar 4;36(1):134–139. doi: 10.1590/S1415-47572013005000002

Figure 1.

Figure 1

Telmisartan and rosiglitazone induce PPARγ transcriptional activation and differentiation of adipose cells. A. U2OS cells were transiently transfected with a reporter plasmid along with luciferase PPRE-Luc and PPARγ vectors. The cells were then treated with 10 μM telmisartan or 1 μM rosiglitazone. The luciferase activity was normalized using β-Galactosidase expression, and the results were calculated from assays performed in triplicate. B. Differentiation of pre-adipocyte 3T3-L1 cells was induced with a medium containing 1 μM dexamethasone, 0.5 mM 3-isobutyl-1-methylxanthine and either telmisartan (1 μM or 10 μM) or rosiglitazone (1 μM). Triglyceride accumulation was quantified as described in the Materials and Methods section. The data are expressed as the mean ± SE, and represent a minimum of three independent experiments, with each data point run in triplicate for each experiment. Statistical analysis were done by Analysis of Variance (ANOVA) For A: * fold-change in luciferase expression relative to expression in the presence of only the control expression vector p < 0.05; ** fold-change in luciferase expression relative to expression in the presence of only the control expression vector p < 0.01; # fold-change in luciferase expression relative to Rosiglitazone activation in the presence of PPARγ expression vector p < 0.01. For B: *p < 0.05 Rosiglitazone vs. Telmisartan.