Fig. 2. RSV inhibits PDGF-induced VSMCs proliferation and migration.
(A) MTT assay for PDGF-BB-treated VSMCs proliferation. The cells were treated with RSV (10, 20, 40 μM), rapamycin (Ra, 100 nM), and PDGF-BB (25 ng/ml) for 48 h. ****p < 0.0001 vs. Con group, #p < 0.05, ####p < 0.0001 vs. PDGF-BB-treated group. (B) Western blot analysis for the protein expression of PCNA in PDGF-BB-treated VSMCs. The cells were treated with RSV (10, 20 and 40 μM) and PDGF-BB (25 ng/ml) for 48 h. ****p < 0.0001 vs. Con group, ##p < 0.01, ###p < 0.001, ####p < 0.0001 vs. PDGF-BB-treated group. (C) Representative images for RSV and PDGF-BB-treated VSMCs migration. The cells were treated with RSV (10, 20 and 40 μM) and PDGF-BB (25 ng/ml) for 48 h. ****p < 0.0001 vs. Con group, ##p < 0.01, ###p < 0.001 vs. PDGF-BB-treated group. Scale bar: 100 μm. (D) Western blot analysis for the protein expression of MMP-2. The cells were treated with RSV (10, 20 and 40 μM) and PDGF-BB (25 ng/ml) for 48 h. ****p < 0.0001 vs. Con group, ###p < 0.001, ####p < 0.0001 vs. PDGF-BB-treated group. Protein expressions were normalized to β‐actin. Data were analyzed using mean ± SEM. All experimental techniques are described in the Methods section. n = 3 per group. RSV, rosuvastatin; PDGF, platelet-derived growth factor; VSMCs, vascular smooth muscle cells; MTT, 3-(4,5-Dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide; PCNA, proliferating cell nuclear antigen; MMP-2, matrix metalloproteinase-2.
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