Qi Dan Li Xin pill improves chronic heart failure by regulating mTOR/p70S6k-mediated autophagy and inhibiting apoptosis

Figures

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  Figure 1. (Fan). Representative echocardiographic images (m-mode) in various groups. Compared with sham animals, the model group showed overtly damaged left ventricular diastolic and systolic functions, significantly weakened cardiac compliance, strengthened myocardial hardness, and obvious ventricular remodeling. However, QD significantly delayed ventricular remodeling, and progressive deterioration of heart function was effectively inhibited.

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  Figure 2. (Fan). Effects of QD on rat heart function. (A) LVEF, LV ejection fraction; LVFS, (B) LVESD, LV fractional; (C) LV end-systolic diameter; (D) LVEED, LV end-diastolic diameter; (E) LVvol;s, LV end-systolic volume; (F) LVvol;d, LV end-diastolic volume. n = 6/group. Data are mean ± s.d.; **P < 0.01 versus sham group; #P < 0.05 and ##P < 0.01 versus model group.

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  Figure 3. (Fan). Quantitative evaluation of hemodynamic properties of the heart. Heart rate (HR) (A), stroke volume (SV) (B), left ventricular systolic pressure (LVSP) (C), left ventricular maximum descent velocity (−dp/dt max) (D), and left ventricular maximum upstroke velocity (+dp/dt max) (E) were assessed. n = 6/group. Data are mean ± s.d. **P < 0.01 versus sham group; #P < 0.05 and ##P < 0.01 versus model group.

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  Figure 4. (Fan). Histopathological assessment of the left ventricle at 28 days post-CHF induction. In rats with myocardial infarction, more fibroblasts at the edge of the infarcted area showed hyperplasia, more live myocardial cells displayed hypertrophy, and less mononuclear cell infiltration was observed compared with the sham group. In the QD groups, fibroblast amounts were obviously reduced at the edge of the infarcted area, with decreased inflammatory cell infiltration, in comparison with the model group (magnification, 400×).

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  Figure 5. (Fan). Cardiac IL-1β, IL-6, TNF-α and IL-10 mRNA amounts in rats 28 days post-CHF induction. Gene expression was examined by qRT-PCR. n = 3 per group. GAPDH was employed for normalization. Data are mean ± s.d. **P < 0.01 versus sham group; #P < 0.05, ##P < 0.01 versus model group.

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  Figure 6. (Fan). Protein amounts of apoptosis-associated molecules. (A) Representative immunoblot bands of various proteins. (B–F) Semi-quantitative evaluation of caspase3, cleaved-caspase3, Bax, Bcl-2 and Bcl-2/Bax in various groups. Data are mean ± s.d. *P < 0.05, **P < 0.01 versus sham group; #P < 0.05, ##P < 0.01 versus model group (n = 3 per group).

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  Figure 7. (Fan). Protein amounts of autophagy-associated molecules. (A) Representative immunoblot bands of various proteins. (B) Semi-quantitative evaluation of LC3-II/LC3-I in various groups. Data are mean ± s.d. *P < 0.05, **P < 0.01 versus sham group; #P < 0.05, ##P < 0.01 versus model group (n = 3 per group).

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  Figure 8. (Fan). Protein amounts of mTOR pathway effectors. (A) Representative immunoblot bands of various proteins. (B–H) Semi-quantitative assessment of mTOR, P-mTOR, p70S6k, P-p70S6k (S371), P-p70S6k (T389), 4E-BP1, P-4E-BP1. Data are mean ± s.d. *P < 0.05, **P < 0.01 versus sham group; #P < 0.05, ##P < 0.01 versus model group (n = 3, each group).