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. 2021 Oct 14;36(5):1095–1110. doi: 10.3803/EnM.2021.1155

Fig. 6.

Fig. 6

Effects of lobeglitazone (LGZ) inhibition of phosphorylation of p38 mitogen-activated protein kinase (MAPK) and matrix metalloproteinase 2 (MMP-2) expression induced by transforming growth factor-beta1 (TGF-β1) are peroxisome proliferator-activated receptor gamma (PPAR-γ) dependent. (A) Western blot showing the effect of GW9662 on LGZ-mediated inhibition of the TGF-β1 activation of p38 MAPK and MMP-2 expression in papillary thyroid carcinoma (PTC) cells. PTC cells are pre-treated with GW9662 for 2 hours and cells are treated with presence or absence of LGZ 5 μM for 30 minutes, then stimulated with TGF-β1 (20 ng/mL) for 15 minutes. (B) The effect of GW9662 on LGZ-mediated inhibition of TGF-β1-induced MMP-2 protein expression in PTC cells by Western blot assay. PTC cells are pre-treated with GW9662 for 2 hours and cells are treated with presence or absence of LGZ 5 μM for 30 minutes, then stimulated with TGF-β1 at the indicated concentrations for 24 and 48 hours. Relative protein expression rate is normalized using β-actin as a loading control. Statistical analysis was performed using the Student’s t test from three independent experiments repeated in triplicates; Error bars correspond to the standard error of the mean; P values are indicated in each panel. aP<0.05 vs. control; bP<0.05 vs. TGF-β1-treated; cP<0.05 vs. TGF-β1 with LGZ-treated.