Key result
Rapamycin dose-dependently improves cardiac function and reduces myocardial apoptosis in heart failure rats.
Why the study?
Does rapamycin improve cardiac function and reduce myocardial cell apoptosis in rats with early heart failure?
Does rapamycin improve cardiac function and reduce myocardial cell apoptosis in rats with early heart failure?
Rapamycin protects against myocardial hypertrophy and apoptosis in a rat model of early heart failure in a dose-dependent manner.
Hypothesis-generating for rapamycin in early HF; leaves open translation to human patients.
OBJECTIVES: Heart failure (HF) progression can be prevented by an inhibitor of the mammalian target of rapamycin and an autophagy enhancer rapamycin. This current study aimed to investigate the effect of rapamycin on HF progression and myocardial cells apoptosis. METHODS: HF rats were injected with low-, middle-, and high-dose rapamycin. Echocardiography, hematoxylin-eosin staining, plasma brain natriuretic peptide, myocardial cells apoptosis, and Akt activation in rapamycin-treated rats were detected. RESULTS: HF rats showed reduced cardiac functions, destructive pathological changes in the myocardium, enhanced Akt activation and myocardial cells apoptosis. However, rapamycin reversed all the changes in a dose-dependent manner. Cardiac functions were enhanced by rapamycin. Myocardial cells apoptotic percentage, Akt expression, and pathological changes of the myocardium in HF rats were inhibited by rapamycin administration. CONCLUSIONS: Rapamycin protected against myocardial hypertrophy and myocardial cells apoptosis in HF rats in a dose-dependent manner.
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Zhang et al. (2018) studied Early heart failure. Rapamycin was evaluated on Cardiac functions, myocardial cells apoptosis, and Akt activation. Rapamycin administration in heart failure rats dose-dependently enhanced cardiac functions and inhibited myocardial cell apoptosis, Akt expression, and pathological myocardial changes.
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