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Fig. 7 | Cellular & Molecular Biology Letters

Fig. 7

From: Disrupted cardiac fibroblast BCAA catabolism contributes to diabetic cardiomyopathy via a periostin/NAP1L2/SIRT3 axis

Fig. 7

Chemical screening showing that GA improved DCM by directly targeted and inhibited perisotin expression in mice. A, B Left ventricle EF and FS were quantified. C Representative echocardiographic images showing the effects of perisotin knockdown on cardiac function in control and diabetic mice. D Serum LDH levels in mice. E Serum CK-MB levels in mice. F, I Representative photographs of the myocardium with H&E staining (Scale bar = 100 μm). G, J Representative photographs of the myocardium with Sirus red staining (Scale bar = 100 μm). H, K Representative images of the myocardium with DHE staining (Scale bar = 200 μm). L The mRNA levels of pro-hypertrophic genes (ANP, BNP, β-MHC) and pro-fibrogenic genes (Col I, Col III, α-SMA). M Representative blots and quantitation of α-SMA, collagen I, and NAP1L2. n = 4–6. *P < 0.05 versus Con, †P < 0.05 versus Diabetes. Differences between groups were assessed with ANOVA followed by Bonferroni post-hoc test (D–I)

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