Hydrogen rescues vascular endothelial cells in obstructive sleep apnea-hypopnea syndrome by modulating nitric oxide.
Qi Chen, Dandan Jiang, Jie He, Mili Sun · Journal of thoracic disease · 2025
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 The researchers employed a translational approach using both in vitro and in vivo models of IH, H₂ administration attenuated vascular remodeling, reducing medial thickening and collagen deposition, and suppressed the inflammatory response by downregulating TNF-α and ICAM-1 expression. These findings from a laboratory model add evidence supporting molecular hydrogen's biological and therapeutic potential in the model studied.
What the Findings Mean
H2HUBB reviewed how hydrogen-rich medium affected the outcomes measured in The researchers employed a translational approach using both in vitro and in vivo models of IH. H₂ administration attenuated vascular remodeling, reducing medial thickening and collagen deposition, and suppressed the inflammatory response by downregulating TNF-α and ICAM-1 expression.
What the Researchers Studied
The researchers studied The researchers employed a translational approach using both in vitro and in vivo models of IH. The study used a in vitro cell-culture laboratory experiment. The comparison condition was control condition or baseline measurements.
What Effects Did Molecular Hydrogen Have?
Source-reported hydrogen concentration: 2% source-reported H₂ gas concentration; Source-reported hydrogen exposure: 2% source-reported H₂ gas concentration; 1 L/min H₂ flow (1000 mL/min H₂); reported treatment duration: 1 hour. H₂ administration attenuated vascular remodeling, reducing medial thickening and collagen deposition, and suppressed the inflammatory response by downregulating TNF-α and ICAM-1 expression. The authors concluded that H₂ effectively alleviates OSAHS-related endothelial dysfunction by modulating redox homeostasis, recoupling eNOS to enhance NO production, and concurrently inhibiting inflammatory activation and apoptosis. Molecular hydrogen (H₂) has emerged as a selective antioxidant with therapeutic potential, but its protective mechanisms against OSAHS-induced endothelial injury remain largely unexplored. Figure 1 Hydrogen alleviates IH-induced oxidative stress in endothelial cells and OSAHS rats. (A) Intracellular ROS in HUVECs under normoxia (Control), intermittent hypoxia (IH), and IH with hydrogen-rich medium (IH + H₂ ) was quantified using DCFH-DA fluorescence.
Why These Findings Matter
These findings from a laboratory model add evidence supporting molecular hydrogen's biological and therapeutic potential in the model studied.
How Strong Is This Evidence?
This is laboratory evidence from a in vitro cell-culture laboratory experiment. It is most informative for the biological mechanisms, cellular responses, or biochemical outcomes directly measured.
Technical Study Details
H2HUBB classifies this publication as laboratory study with laboratory or cellular evidence. The research population or model was The researchers employed a translational approach using both in vitro and in vivo models of IH. The study used a in vitro cell-culture laboratory experiment. The hydrogen delivery method was hydrogen-rich medium. The source-reported hydrogen concentration was 2% source-reported H₂ gas concentration. The reported treatment duration was 1 hour.
Limitations and Safety
No separate limitations or safety findings were identified in the current-study 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.