Figure 4 | Scientific Reports

Figure 4

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

Figure 4

Thalidomide (THL) inhibits TGF-β1-mediated phosphorylation of MAPK in CCL-149 cells. (A) Cells were preincubated for 1 h with JNK inhibitor SP600125 (10 μM), ERK inhibitor PD098059 (40 μM), and p38 inhibitor SB203580 (20 μM) and then stimulated with TGF-β1 (5 ng/mL) for 48 h. Then, cells were collected for α-SMA measurement by western blot. (B,C and D) Following TGF-β1 treatment, JNK, ERK and p38 were markedly phosphorylated in CCL-149 cells. Treatment with THL (1, 10, or 100 μg/mL) or SB431542 (5 μM) attenuated JNK, ERK and p38 phosphorylation. β-Actin was used as a loading control. Data are expressed as the means ± SD, and n = 3 in each group. THL: thalidomide; SB431542: TGF-β1R-Kinase inhibitor; α-SMA: α-smooth muscle actin; ##p < 0.01 compared to the TGF-β1 group (untreated); **p < 0.01 compared to all other groups.

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