Astragaloside IV inhibits ventricular remodeling and improves fatty acid utilization in rats with chronic heart failure

Figures

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  Figure 1. The UCG result of the sham operation rats and the AAC rats (n=20 for the CHF + Benazepril HCL group, the sham operation group and the CHF + high-dose group, n=18 for the CHF model group and n=19 for the CHF+low-dose group) (A–C) Compared with the sham operation rats, the LVEDD, LVESD, LVPWD, and IVRT of the AAC rats increased, while the LVEF, LVFS, and E/A of the AAC rats decreased. bP<0.05 compared with sham operation rats, cP<0.01 compared with sham operation rats. (D) The serum FFA concentration of the AAC rats increased compared with the sham operation rats. (E,F) Representative M-mode LV echocardiographs and mitral velocity profiles of the five groups of rats.

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  Figure 2. The results after AS-IV intervention. Representative M-mode LV echocardiographs (A), mitral velocity profiles (B), and left ventricular pressure waveform (C) of the five experimental groups after intervention (n=20 for the CHF + Benazepril HCL group, the sham operation group, and the CHF + high-dose group, n=18 for the CHF model group and n=19 for the CHF + low-dose group).

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  Figure 3. LVMI and HMI and Grossmorphology. The results of the LVMI (A) and HMI (B) measurement after different interventions (n=20 for the CHF + Benazepril HCL group, the sham operation group, and the CHF + high-dose group, n=18 for the CHF model group, and n=19 for CHF + low-dose group). Representative gross morphology of the whole hearts (C) and the corresponding transverse cross-sections at the mid-ventricle level (D). cP<0.01 comapred with the sham operation, eP<0.05 compared with the CHF model, fP<0.01 compared with the CHF model.

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  Figure 4. The serum and myocardium FFA concentration. Serum FFA concentration (A) and myocardium FFA concentration (B) of the five experimental groups. The quantitative data are shown as the means ± S.D. (n=20 for the CHF + Benazepril HCL group, the sham operation group, and the CHF + high-dose group, n=18 for the CHF model group and n=19 for the CHF + low-dose group); cP<0.01 compared with the sham operation, eP<0.05, fP<0.01 compared with the CHF model.

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  Figure 5. Representative staining sections of the five experimental groups after the interventions (n=20 for the CHF + Benazepril HCL group, the sham operation group, and the CHF + high-dose group, n=18 for the CHF model group and n=19 for the CHF + low-dose group) The sections were visualized at 200× magnification. (A) The sections were stained with H&E. (B) The sections were stained using Masson’s trichrome. Red indicates the muscle fibers and blue indicates collagen. (C) Myocyte cross-sectional area date. (D) CVF of the quantitative data. cP <0.01 compared with the sham operation, eP<0.05, fP<0.01 compared with the CHF model.

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  Figure 6. Expression analysis of key enzymes involved in FFA metabolism. Representative blots of PPARα, MCAD, and MCPT1 (A) and the intensity normalized against GAPDH (B) in the LV myocardium of the five groups (n=20 for the CHF + Benazepril HCL group, the sham operation group, and the CHF + high-dose group, n=18 for the CHF model group and n=19 for the CHF + low-dose group). The quantitative data are given as the means ± S.D. cP<0.01 compared with the sham operation; eP<0.05, fP<0.01 compared with the CHF model.

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  Figure 7. Relative quantitation of PPARα, MCAD, and MCPT1 mRNA by RT-qPCR in the myocardia of the five groups of rats (n=20 for CHF + Benazepril HCL group, the sham operation group, and the CHF + high-dose group, n=18 for the CHF model group and n=19 for the CHF + low-dose group) The quantitative data are given as the means ± S.D. cP<0.01 compared with the sham operation; eP<0.05, fP<0.01 compared with the CHF model. Please note that compared with the sham operation group, CHF + low-dose group was still statistically significant (P<0.05); however, the difference in the CHF + high-dose group compared with the sham control group was not significant (P>0.05).