Smad3 signaling pathway, ECM-related genes and miR-29b expression in rat cardiac fibroblasts.

<p>A. Measurement of intracellular ROS by DCFH-DA staining (400× magnification). The figures are representative of three independent experiments. ^#<i>p</i> <0.001 vs. Blank, ^&<i>p</i> <0.001 vs. Ang II, N=4. B. Inactivation of smad3 in NAC- and carvedilol-treated rat cardiac fibroblasts. ^#<i>p</i> <0.05 vs. Blank, *<i>p</i> <0.05 vs. Ang II, N=4. C. Downregulation of Col1a1, Col3a1, and α-SMA in smad3 knockdown rat cardiac fibroblasts. *<i>p</i> < 0.05, **<i>p</i> < 0.01 vs. control group, N = 4. D. Upregulation of mature miR-29b in smad3 knockdown rat cardiac fibroblasts. *<i>p</i> < 0.05, **<i>p</i> < 0.01 vs. control group, N = 4. E. Upregulation of miR-29b-2 precursor in smad3 knockdown rat cardiac fibroblasts. ^※<i>p</i> < 0.01 vs. miR-29b-1 in control group, ^#<i>p</i> < 0.01 vs. control group, N = 4. F. Downregulation of Col1a1, Col3a1, and α-SMA in SIS-3 or Nar-treated rat cardiac fibroblasts. *<i>p</i> < 0.05, **<i>p</i> < 0.01, ***<i>p</i> < 0.001 vs. Blank group, N = 4. G. Upregulation of mature miR-29b in SIS-3 or Nar-treated rat cardiac fibroblasts. *<i>p</i> < 0.05, **<i>p</i> < 0.01 vs. control group, N = 4. H. Upregulation of miR-29b-2 precursor in SIS-3 or Nar-treated rat cardiac fibroblasts. ^※<i>p</i> < 0.01 vs. miR-29b-1 in blank control group, *<i>p</i> < 0.05, **<i>p</i> < 0.01 vs. miR-29b-2 in blank control group, N = 4.