Figure 1 | Scientific Reports

Figure 1

From: Thalidomide Inhibits TGF-β1-induced Epithelial to Mesenchymal Transition in Alveolar Epithelial Cells via Smad-Dependent and Smad-Independent Signaling Pathways

Figure 1

Thalidomide (THL) attenuates TGF-β1-induced EMT in CCL-149 cells. (A) Morphological changes (200×) in CCL-149 cells treated with vehicle or TGF-β1 (5 ng/mL) for 48 hours in the presence of vehicle (DMSO), SB431542 (5 μM), or THL (100 μg/mL). (B) CCL-149 cells stimulated with TGF-β1 (5 ng/mL) were treated with THL (1, 10, or 100 μg/mL) or SB431542 (5 μM) for 48 hours, and the lysates were analyzed for ZO-1, E-Cadherin, α-SMA and vimentin. β-Actin was used as the loading control. Data are expressed as the means ± SD, and n = 3 in each group. THL: thalidomide; SB: SB431542, TGF-β1R-Kinase inhibitor; ZO-1: zonula occludens-1; α-SMA: α-smooth muscle actin; #p < 0.05, ##p < 0.01 compared to the TGF-β1 group (untreated); *p < 0.05, **p < 0.01 compared to all other groups.

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