Protective effects of molecular hydrogen on lung injury from lung transplantation.
Lini Quan, Bin Zheng, Huacheng Zhou · Experimental biology and medicine (Maywood, N.J.) · 2021
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
This narrative review examined the available molecular-hydrogen literature. Taken together, accumulating experimental evidence indicates that H₂ can significantly alleviate transplantation-related lung injury, mainly via inhibition of inflammatory cytokine secretion and reduction in oxidative stress through several underlying mechanisms. The reviewed evidence adds support for molecular hydrogen's therapeutic potential across the conditions, mechanisms, or outcomes examined.
What the Findings Mean
H2HUBB reviewed this publication as a synthesis of molecular-hydrogen research and summarizes the outcomes emphasized by the authors. 12 In a rat model of LTx wherein both brain dead donors and recipients received 2% hydrogen ventilation, the researchers found that hydrogen treatment could decrease the IL-8, TNF- a and intracellular adhesion molecule (ICAM)-1 levels, increase SOD activity and reduce MDA levels, and mitigate apopto- sis in lung grafts, leading to improved PaO 2/FiO2 ratio, static compliance, and graft histology.
What the Researchers Studied
The authors reviewed protective effects of molecular hydrogen on lung injury from lung transplantation.
What Effects Did Molecular Hydrogen Have?
55 The mechanism of antioxidant effects of molecular hydrogen was shown to involve in the activation of Nrf2 signaling pathway in lung injury induced by hyperoxia, 36 seawater instillation,56 sepsis,57 and paraquat-induced lung fibroblast injury in vitro.58 Hydrogen was shown to increase pulmonary HO-1 protein and mRNA expression, as well as HO-1 activity in the lungs of rats exposed to hyperoxia. 12 In a rat model of LTx wherein both brain dead donors and recipients received 2% hydrogen ventilation, the researchers found that hydrogen treatment could decrease the IL-8, TNF- a and intracellular adhesion molecule (ICAM)-1 levels, increase SOD activity and reduce MDA levels, and mitigate apopto- sis in lung grafts, leading to improved PaO 2/FiO2 ratio, static compliance, and graft histology. The authors concluded that taken together, accumulating experimental evidence indicates that H₂ can significantly alleviate transplantation-related lung injury, mainly via inhibition of inflammatory cytokine secretion and reduction in oxidative stress through several underlying mechanisms. Hydrogen precon- ditioning alleviated cardiac death lung graft I/R injury by reducing inflammatory mediator upregulation, demon- strated by decreased myeloperoxidase (MPO) activity, lower serum interleukin (IL)-6 and tumor necrosis factor (TNF)-a levels, and elevated IL-10 level. Hydrogen was also shown to attenuate oxidative stress evidenced by increased superoxide dismutase (SOD) activity and a decreased malondialdehyde (MDA) level, and to decrease the alveolar epithelia cellular apoptosis in lung grafts.
Why These Findings Matter
The reviewed evidence adds support for molecular hydrogen's therapeutic potential across the conditions, mechanisms, or outcomes examined.
How Strong Is This Evidence?
This is review or synthesis evidence (narrative review).
Technical Study Details
H2HUBB classifies this publication as narrative review with review or synthesis evidence. The study used a narrative review. The hydrogen delivery method was hydrogen-rich water.
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. The original scholarly source is available at https://www.ebm-journal.org/journals/experimental-biology-and-medicine/articles/10.1177/15353702211007084/pdf.