Hydrogen therapy: from mechanism to cerebral diseases.
Cheng-Lin Liu, Kai Zhang, Gang Chen · Medical gas research · 2016
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. The medicinal value of hydrogen (H₂) was ignored prior to research illustrating that inhalation of 2% H₂ can significantly decrease the damage of cerebral ischemia/reperfusion caused by oxidative stress via selective elimination of hydroxyl freebase (OH) and peroxynitrite anion (ONOO-). 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. The medicinal value of hydrogen (H₂) was ignored prior to research illustrating that inhalation of 2% H₂ can significantly decrease the damage of cerebral ischemia/reperfusion caused by oxidative stress via selective elimination of hydroxyl freebase (OH) and peroxynitrite anion (ONOO-).
What the Researchers Studied
The authors reviewed hydrogen therapy: from mechanism to cerebral diseases.
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. The medicinal value of hydrogen (H₂) was ignored prior to research illustrating that inhalation of 2% H₂ can significantly decrease the damage of cerebral ischemia/reperfusion caused by oxidative stress via selective elimination of hydroxyl freebase (OH) and peroxynitrite anion (ONOO-). The authors concluded that it is important to note that underlying mechanisms, optimal concentration, and biological safety of H₂ are worthy of deeper investigation. H₂: hydrogen; •OH: hydroxyl freebase; ONOOˉ: peroxynitrite anion; BBB: blood brain barrier; IL-1β: interleukin 1 beta; TNF-α: tumor necrosis factor-alpha; DR: death receptors; TRAIL: TNF related apoptosis inducing ligand; TUNEL: Terminal-deoxynucleotidyl Transferase Mediated Nick End Labeling; NF-κB: Nuclear factor-κB; ERK 1/2: extracellular-regulated kinase1/2; DNA: deoxyribonucleic acid; ROS: reactive oxygen species; tMCAO: transient middle cerebral artery occlusion; pMCAO: persistent middle cerebral artery occlusion; 8-OhdG: 8-hydroxy-2-deoxyguanosine; MMP-9: matrix metalloproteinases-9; SAH: subarachnoid hemorrhage; ICH: intracerebral hemorrhage; Hb: hemoglobin; TBI: Traumatic brain injury; AD: Alzheimer's disease; PD: Parkinson's disease; SOD: superoxide dismutase; MDA: malondialdehyde; NHI: neonatal hypoxia-ischemia.
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 inhaled hydrogen gas. The source-reported hydrogen concentration was 2% source-reported H₂ gas concentration.
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.