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. Author manuscript; available in PMC: 2019 Jan 15.
Published in final edited form as: Toxicology. 2017 Nov 7;393:150–159. doi: 10.1016/j.tox.2017.11.010

Figure 2. Pyraclostrobin-induced TG accumulation is independent of PPARγ activity.

Figure 2

(A) Rosiglitazone (RSG) (one-way ANOVA (p<0.0001), N=4), but not pyraclostrobin (PYRA) (one-way ANOVA (p=0.89), N=4), increased PPARγ activity in a dose-dependent manner utilizing the Invitrogen GeneBLAzer PPARγ FRET reporter assay. Exposure to pyraclostrobin reduced (B) PPARγ (one-way ANOVA (p<0.0001), N=6), (C) Cebpα (transcription factor that regulates adipogenesis; one-way ANOVA (p<0.0001), N=6), and (D) Lpl (adipocyte marker; one-way ANOVA (p<0.0001), N=6) mRNA expression, while rosiglitazone increased the expression of all genes in Zenbio 3T3-L1 cells after ten days of differentiation. (E) The PPARγ antagonists GW9662 and T0070907 reduce RSG-induced TG accumulation (one-way ANOVA (p=0.02), N=3), while having no effect on PYRA-induced TG accumulation (one-way ANOVA (p=0.38), N=3). Asterisk denotes statistical significance (p<0.05) for post-hoc comparison (Dunnett’s test) to control. Bars±SEM.