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. Author manuscript; available in PMC: 2015 Dec 18.
Published in final edited form as: Chem Biol Interact. 2014 Nov 6;225:90–98. doi: 10.1016/j.cbi.2014.10.032

Fig. 1.

Fig. 1

ER stress response in cardiac apoptosis and fibrosis after MI. (A) Western blots and quantitative analysis of ER stress response markers (GRP 78 and CHOP) in the whole heart homogenates of mice in the early and late phase of MI. (B) Western blots and quantitative analysis of pro-apoptotic proteins (Bax and caspase 3) in the whole heart homogenates of mice in the early and late phase of MI. (C) Western blots and quantitative analysis of pro-fibrotic proteins (TGF-β1 and Smad 2/3) in the whole heart homogenates of mice in the early and late phase of MI. (D) Representative Western blots and quantitative analysis of CHOP, Bax and caspase 3 from whole heart homogenates at 3rd day of MI with or without 4-PBA (20 mg/kg/d). (E) Representative Western blots and quantitative analysis of CHOP, TGF-β1 and Smad 2/3 from whole heart homogenates at 28th day of MI with or without 4-PBA (20 mg/kg/d). #P < 0.05 vs. sham; †P < 0.05 vs. MI; n = 4–6 in each group.