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. 2015 Jun 24;4(7):e001598. doi: 10.1161/JAHA.114.001598

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© 2015 The Authors. Published on behalf of the American Heart Association, Inc., by Wiley Blackwell.

This is an open access article under the terms of the Creative Commons Attribution-NonCommercial License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited and is not used for commercial purposes.

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Apocynin attenuated cardiac fibrosis via inhibiting extracellular signal-regulated kinase 1/2 activation and fibroblast growth factor-2 expression. A, Ang II–induced ERK1/2 p-ERK was inhibited by apocynin. B and C, Ang II–induced expressions of FGF-2 and fibrosis biomarkers, including procollagen I procollagen III and TGF-β, were reduced by U0126 (ERK1/2 inhibitor) in cardiac fibroblasts. Data were expressed as mean±SD; n=3 for each group. *P<0.01 vs Control group; ^#P<0.01 vs Ang II group. Ang II indicates angiotensin II; p-ERK, phosphorylation extracellular signal-regulated kinase; FGF-2, fibroblast growth factor-2; TGF-β, transforming growth factor-beta; GAPDH, anti–glyceraldehyde 3-phosphate dehydrogenase; ERK1/2, extracellular signal-regulated kinase 1/2.