Inhalation of Hydrogen Attenuates Progression of Chronic Heart Failure via Suppression of Oxidative Stress and P53 Related to Apoptosis Pathway in Rats.
Jing Chi, Zizhuo Li, Xiaojian Hong, Tong Zhao, Yueyue Bie, Wen Zhang, Jiaxing Yang, Ziming Feng, Zhouqi Yu, Qiannan Xu, Luqi Zhao, Weifan Liu, Yunan Gao, Hongxiao Yang, Jiemei Yang, Jiaren Liu, Wei Yang · Frontiers in physiology · 2018
Research-use notice
Independent study record
Each H2HUBB study page organizes source-linked research details for educational use. Interpretation should remain proportional to the study design, population, controls, and limitations.
H2HUBB TAKEAWAY
In rats, 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). These preclinical findings add evidence supporting molecular hydrogen's therapeutic potential within the outcomes and biological pathways measured in this model.
What the Findings Mean
H2HUBB reviewed how hydrogen-rich water affected the outcomes measured in rats. 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).
What the Researchers Studied
The researchers studied rats. The study used a preclinical animal experiment. The comparison condition was control condition or baseline measurements.
What Effects Did Molecular Hydrogen Have?
Rats were separated into four groups at random (15/group): Sham, rats treated with H₂, CHF and CHF treated with H₂ ( Figure 1 ). Then cells were treated with hydrogen for 2 h, 4 h, 6 h, 8 h, 12 h, 24 h, and 72 h. With optical microscope, cells were observed when treated with hydrogen until all died (72 h); cells died partially were treated with hydrogen for 24 h, and cells in good conditions were treated with hydrogen for 2 h, 4 h, 6 h, 8 h, and 12 h. 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). The authors concluded that 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. Modulatory effects of molecular hydrogen on apoptosis were also determined in cultured primary cardiomyocytes that underwent oxidative stress injury ( Figures 7A,B ).
Why These Findings Matter
These preclinical findings add evidence supporting molecular hydrogen's therapeutic potential within the outcomes and biological pathways measured in this model.
How Strong Is This Evidence?
This is preclinical animal evidence from a preclinical animal experiment. It is most informative for the disease model, mechanisms, biomarkers, and outcomes directly measured in the study.
Technical Study Details
H2HUBB classifies this publication as animal study with preclinical animal evidence. The research population or model was rats. The study used a preclinical animal experiment. The hydrogen delivery method was hydrogen-rich water.
Limitations and Safety
Safety information: As a safe antioxidant, molecular hydrogen mitigates the progression of CHF via inhibiting apoptosis modulated by p53. the safety of molecular hydrogen to cardiomyocytes has been confirmed as reported before ( Tao et al., 2015 ). Inhalation of H₂ may be a safe and effective therapy for CHF, and may be applied to patients with CHF.
Original Study and H2HUBB Research Context
H2HUBB presents this source-grounded research record as one contribution to the broader molecular-hydrogen evidence base.