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. 2018 Dec 11;39:83–94. doi: 10.1016/j.ebiom.2018.12.003

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© 2018 The Authors

This is an open access article under the CC BY license (http://creativecommons.org/licenses/by/4.0/).

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Fig. 7 — Inhibiting Foxm1 activity abolished the heart protective role of VPA after MI. (a) qPCR validation of genes regulated by VPA treatment after MI in rats. (b) qPCR analysis of VPA regulated genes in Foxm1 overexpression MI mice. *, P < .05 vs Sham group; **, P < .01 vs Sham group; #, P < .05 vs MI group; ##, P < .01 vs MI group; n = 3. (c) and (d) Echocardiographic measurements of ejection fraction (EF) and fractional shortening (FS) of Sham, MI, MI + VPA, MI + TST and MI + VPA + TST rats at 24 h after MI. *, P < .05 vs MI group; #, P < .05 vs MI + VPA group; n = 3. (e) Representative images of heart sections by TTC staining. Scale bar: 2.5 mm (f) Quantitative analysis of infarct size expressed as percentage of left ventricle. *, P < .05 vs MI group; #, P < .05 vs MI + VPA group; n = 3. All samples were analyzed by one way ANOVA followed by post-hoc Turkey HSD analysis. Data were expressed as mean ± SEM.