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. 2021 Mar 26;23(6):404. doi: 10.3892/mmr.2021.12043

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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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Figure 5. — Nox4 overexpression reverses the effects of TIIA in improving cardiac dysfunction on rats with MI-induced heart failure. (A) The expression level of Nox4 was increased in the heart rats treated with adenoviral (Ad)-Nox4. (B) Nox4 overexpression reversed the improving effects of TIIA on the decreases of LV ± dp/dt_max in MI rats. (C) Nox4 overexpression reversed the improving effects of TIIA on the decreases of LV EF, FS and LVSP and the increases of LVVS, LVVD, LVESD and LVEDD in MI rats. The results are expressed as mean ± standard error of the mean. n=8. *P<0.05 vs. the (A) Ad-GFP or (B and C) Sham + Ad-GFP group; #P<0.05 vs. the MI + Ad-GFP group; &P<0.05 vs. the MI + TIIA group. Nox, NADPH oxidase; TIIA, tanshinone IIA; MI, myocardial infarction; LV ± dp/dt_max, maximum of the first differentiation of LV pressure; LV, left ventricular; EF, ejection fraction; FS, fractional shortening; LVSP, LV systolic pressure; LVVS, LV volume in systole; LVVD, LV volume in diastole; LVESD, LV end-systolic diameter; LVEDD, LV end-diastolic diameter.