Inhalation of Hydrogen Attenuates Progression of Chronic Heart Failure via Suppression of Oxidative Stress and P53 Related to Apoptosis Pathway in Rats

• Published in: Frontiers in physiology Vol. 9; p. 1026
• Main Authors: Chi, Jing, Li, Zizhuo, Hong, Xiaojian, Zhao, Tong, Bie, Yueyue, Zhang, Wen, Yang, Jiaxing, Feng, Ziming, Yu, Zhouqi, Xu, Qiannan, Zhao, Luqi, Liu, Weifan, Gao, Yunan, Yang, Hongxiao, Yang, Jiemei, Liu, Jiaren, Yang, Wei
• Format: Journal Article
• Language: English
• Published: Switzerland Frontiers Media S.A 31.07.2018
• Subjects: apoptosis; chronic heart failure; hydrogen; oxidative stress; p53; Physiology; apoptosis; chronic heart failure; hydrogen; oxidative stress; p53
• ISSN: 1664-042X; 1664-042X
• DOI: 10.3389/fphys.2018.01026

Continuous damage from oxidative stress and apoptosis are the important mechanisms that facilitate chronic heart failure (CHF). Molecular hydrogen (H ) has potentiality in the aspects of anti-oxidation. The objectives of this study were to investigate the possible mechanism of H inhalation in delaying the progress of CHF. A total of 60 Sprague-Dawley (SD) rats were randomly divided into four groups: Sham, Sham treated with H , CHF and CHF treated with H . Rats from CHF and CHF treated with H 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 H , cardiac function was improved vs. CHF ( < 0.05), whereas oxidative stress damage and apoptosis were significantly attenuated ( < 0.05). In this study, the mild oxidative stress was induced in primary cardiomyocytes of rats, and H treatments significantly reduced oxidative stress damage and apoptosis in cardiomyocytes ( < 0.05 or < 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 H treatment in this rat model and H9c2 cells ( < 0.05 or < 0.01). 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, H is equipped with potential therapeutic application as a novel antioxidant in protecting CHF in the future.