Hydrogen‑rich solution against myocardial injury and aquaporin expression via the PI3K/Akt signaling pathway during cardiopulmonary bypass in rats.
Dandan Song, Xuelei Liu, Yugang Diao, Yingjie Sun, Guangjie Gao, Tiezheng Zhang, Keyan Chen, Ling Pei · Molecular medicine reports · 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 Sprague Dawley rats, hRS treatment significantly increased the viability of myocardial cells, reduced the rate of myocardial cellular apoptosis and the release of MDA and LDH compared with the CPB group. 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 molecular hydrogen affected the outcomes measured in Sprague Dawley rats. HRS treatment significantly increased the viability of myocardial cells, reduced the rate of myocardial cellular apoptosis and the release of MDA and LDH compared with the CPB group.
What the Researchers Studied
The researchers studied Sprague Dawley rats. The study used a preclinical animal experiment.
What Effects Did Molecular Hydrogen Have?
The aim of the present study was to investigate the effects of hydrogen‐rich solution (HRS) and aquaporin (AQP) on cardiopulmonary bypass (CPB)‐induced myocardial injury, and determine the mechanism of the phosphatidylinositol 3‐kinase (PI3K)/protein kinase B (Akt) signaling pathway. The levels of myocardial injury markers [adult cardiac troponin I (cTnI), lactate dehydrogenase (LDH), creatine kinase MB (CK‐MB) and brain natriuretic peptide (BNP)], inflammatory factors [interleukin (IL)‐1β, IL‐6 and tumor necrosis factor‐α (TNF‐α)] and oxidative stress indicators [superoxide dismutase (SOD), malondialdehyde (MDA) and myeloperoxidase (MPO)] were determined by ELISA. HRS treatment significantly increased the viability of myocardial cells, reduced the rate of myocardial cellular apoptosis and the release of MDA and LDH compared with the CPB group.
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 Sprague Dawley rats. The study used a preclinical animal experiment.
Limitations and Safety
No separate limitations or safety findings were identified in the source text available to H2HUBB.
Original Study and H2HUBB Research Context
H2HUBB presents this source-grounded research record as one contribution to the broader molecular-hydrogen evidence base.