Tiaoshen Tongluo Attenuates Fibrosis by Modulating the TGF-β1/Smad Pathway in Endometrial Stromal Cells and a Rat Model of Intrauterine Adhesion

Figure 3

Activation of Smad proteins by TGF-β1 in vitro. (a) Representative immunofluorescence-based identification of endometrial stromal cells (ESCs) with or without 50 ng/ml TGF-β1 treatment for 48 h. Images showing vimentin staining (green). Nuclei were counterstained with DAPI (blue). Scale bar = 100 μm. (b–g) The ESCs were treated with 0, 10, 20, 50, and 100 ng/ml TGF-β1 for 48 h. The relative mRNA expression of Smad2 (b), Smad3 (c), Smad4 (d), and Smad7 (e) detected by real-time PCR. (f) The protein expression of Smad2, phosphorylated-Smad2, Smad3, phosphorylated-Smad3, Smad4, and Smad7 detected by Western blot. (g) The protein expression of Smad2, phosphorylated-Smad2, Smad3, phosphorylated-Smad3, Smad4, and Smad7 was quantified relative to that of β-actin.  < 0.05,  < 0.01 compared to control without TGF-β1 (0 ng/ml).

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