Abstract
Background: Continuous damage from oxidative stress and apoptosis are the important mechanisms that facilitate chronic heart failure (CHF). Molecular hydrogen (H2) has potentiality in the aspects of anti-oxidation. The objectives of this study were to investigate the possible mechanism of H2 inhalation in delaying the progress of CHF.Methods and Results: A total of 60 Sprague-Dawley (SD) rats were randomly divided into four groups: Sham, Sham treated with H2, CHF and CHF treated with H2. Rats from CHF and CHF treated with H2 groups were injected isoprenaline subcutaneously to establish the rat CHF model. One month later, the rat with CHF was identified by the echocardiography. After inhalation of H2, cardiac function was improved vs. CHF (p < 0.05), whereas oxidative stress damage and apoptosis were significantly attenuated (p < 0.05). In this study, the mild oxidative stress was induced in primary cardiomyocytes of rats, and H2 treatments significantly reduced oxidative stress damage and apoptosis in cardiomyocytes (p < 0.05 or p < 0.01). Finally, as a pivotal transcription factor in reactive oxygen species (ROS)-apoptosis signaling pathway, the expression and phosphorylation of p53 were significantly reduced by H2 treatment in this rat model and H9c2 cells (p < 0.05 or p < 0.01).Conclusion: As a safe antioxidant, molecular hydrogen mitigates the progression of CHF via inhibiting apoptosis modulated by p53. Therefore, from the translational point of view and speculation, H2 is equipped with potential therapeutic application as a novel antioxidant in protecting CHF in the future.
Highlights
Because chronic heart failure (CHF), the end-stage of various heart diseases, continues to cause substantial morbidity and mortality, the ideally treatment for CHF needs to improve
The left ventricular end-systolic dimension (LVESD), Left ventricular end-diastolic dimension (LVEDD), right atrium vertical diameter (RAVD), right atrium transverse diameter (RATD), interventricular septum (IVS), and right ventricle (RV) dramatically reduced when compared to the CHF group, there were no significant differences between CHF and CHF with H2 group in left ventricular posterior wall (LVPW) and left atrium (LA)
These results collectively suggest that H2 may prevent the development of CHF and protect the cardiac function in rats
Summary
Because chronic heart failure (CHF), the end-stage of various heart diseases, continues to cause substantial morbidity and mortality, the ideally treatment for CHF needs to improve. Apoptosis serves as another mechanism for the aggravation of CHF (Aubert et al, 2013; Li J. et al, 2014; Gorski et al, 2015). Acute oxidative stress causes severe injury to tissues (Kotur-Stevuljevic et al, 2015), and continuous oxidative stress is one of the reasons of abundant chronic diseases, tumor and senility (Sundar et al, 2013; Granados-Principal et al, 2014; Miller and Sadeh, 2014). Bioenergetic activity and mitochondrial dysfunctions result in the generation of excess amounts of oxidant stress and further enhance cardiomyocytes apoptosis (Okonko and Shah, 2015). Continuous damage from oxidative stress and apoptosis are the important mechanisms that facilitate chronic heart failure (CHF). The objectives of this study were to investigate the possible mechanism of H2 inhalation in delaying the progress of CHF
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