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Fig. 1 | BMC Musculoskeletal Disorders

Fig. 1

From: Investigating the effects of Pirfenidone on TGF-β1 stimulated non-SMAD signaling pathways in Dupuytren’s disease -derived fibroblasts

Fig. 1

Pirfenidone significantly reduced TGF-β1-induced phosphorylation of Akt in CT- and DD-derived fibroblasts. a CT- and DD-cord derived fibroblasts derived from three different patient samples (N = 3/group) were maintained in α-MEM medium containing 0.1% dialyzed FBS for 24 h. After 24 h, cells were either left as controls or treated with PFD (800 μg/ml) in the presence or absence of TGF-β1 (10 ng/ml) for an additional 24 h. Cell lysates were subjected to Western blot analyses to determine the expression of phosphorylated Akt. b Densitometry results are reported as the ratio of phosphorylated Akt protein level to GAPDH expression. Values are means ± standard error mean (SEM) of three independent studies from each of CT- and DD- derived fibroblasts. b Shown here is a representative image of Western blots from three different cultures of CT- and DD-cord derived fibroblasts, each showing similar results. ***p < 0.0001, **p < 0.0059. Ntx; No treatment, PFD- Pirfenidone, TGF-β1, T + P; TGF- β1 + Pirfenidone

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