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. 2018 Oct 2;42(6):3083–3092. doi: 10.3892/ijmm.2018.3914

Figure 2.

Figure 2

BML-111 suppressed TGF-β1-induced NIH3T3 cell activation. Cells were pretreated with a vehicle (0.035% ethanol) or BML-111 (200 nM) for 30 min in the absence or presence of BOC-2 (10 µM; administered 30 min prior to BML-111 treatment) and then stimulated with TGF-β1 (5 ng/ml) for 24 h. (A) The protein expression of α-SMA and fibronectin and the results of the western blot analysis quantified for (B) α-SMA and (C) fibronectin; and (D) total collagen concentration and (E) cell viability were assessed. Data are presented as the mean ± standard deviation for three independent experiments. #P<0.05 and ##P<0.01 vs. the vehicle group. *P<0.05 and **P<0.01 vs. the TGF-β1 group in the absence of BML-111. TGF-β1, Transforming growth factor-β1; BOC-2, N-tert-butyloxy-carbonyl-phenyalanine-le-ucyl-phenyalanine-leucyl-phenyalanine; α-SMA, smooth muscle α actin.