Journal: International Journal of Molecular Medicine

Article Title: BML-111 suppresses TGF-β1-induced lung fibroblast activation in vitro and decreases experimental pulmonary fibrosis in vivo

doi: 10.3892/ijmm.2018.3914

Figure Lengend Snippet: BML-111 decreased TGF-β1-induced NIH3T3 cell α-SMA expression in a dose-dependent manner. (A) NIH3T3 cells express rs1 and (B) FPR2. Cells were pretreated with a vehicle (0.035% ethanol) or BML-111 (1, 10, 100, 200 and 500 nM) for 30 min and then treated with TGF-β1 (5 ng/ml) for 24 h. (C) The expression of α-SMA was assessed using western blotting and (D) quantified. Similar results were obtained from at least 3 sections. Data are expressed as the mean ± standard deviation. # 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. Magnification, ×200. TGF-β1, Transforming growth factor-β1; α-SMA, smooth muscle α actin; rs1, related sequence 1; FPR2, formyl peptide receptor; marker 1, Trans DNA ladder (Tiangen Biotech, Co., Ltd., Beijing, China).

Article Snippet: Following permeabilization, washing and blocking, the cells were incubated with rabbit anti-FPR2 anti-bodies (1:100; cat. no. AFR-002; Alomone Labs, Jerusalem, Israel) at 4°C overnight and then washed and incubated with a fluorescent-labeled secondary antibody (fluorescein isothiocyanate-labelled goat anti-rabbit immunoglobulin G; 1:50; cat. no. AS1110; Aspen Biological, Wuhan, China) for 45 min at 37°C.

Techniques: Expressing, Western Blot, Standard Deviation, Sequencing, Marker