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. 2020 Feb 13;45(4):1081–1090. doi: 10.3892/ijmm.2020.4497

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Copyright: © Chen et al.

This is an open access article distributed under the terms of the Creative Commons Attribution-NonCommercial-NoDerivs License, which permits use and distribution in any medium, provided the original work is properly cited, the use is non-commercial and no modifications or adaptations are made.

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(A) Pre-treatment with Gap26 inhibited H9C2 cell apoptosis following Hcy-induced injury. Gap26 was used at 0.5 µmol/l. (B) Statistical analysis of the rate of apoptosis in each group. (C and E) Hcy-induced upregulation of Bax/Bcl-2, cleaved caspase-3 and Cx43 protein levels was prevented by Gap26. (D, F and G) Quantification of Bax/Bcl-2, cleaved caspase-3 and Cx43. (H-J) Hcy-induced upregulation of Bax/Bcl-2, cleaved caspase-3 and Cx43 mRNA levels was prevented by Gap26. ^**P<0.01, ^***P<0.001 vs. control; ^#P<0.05, ^##P<0.01 vs. Hcy treatment. Data are shown as the means ± SE (n=3). Hcy, homocys-teine; PFD, pirfenidone; Cx43, connexin 43.