敗血症関連脳症に対する分子状水素の保護効果：現状のレビュー
Sepsis-associated encephalopathy (SAE) is a serious neurological complication of sepsis, manifesting as cognitive impairment and neurological dysfunction. Its pathophysiology involves oxidative stress, neuroinflammation, mitochondrial dysfunction, and disruption of the blood-brain barrier. This review examines the current body of evidence regarding the neuroprotective potential of molecular hydrogen (H2) in SAE. H2 exerts its effects by scavenging reactive oxygen species, suppressing activation of astrocytes and microglia, and reducing mitochondrial dysfunction, collectively attenuating neuroinflammation and neuronal injury. Variability in dosing, administration routes, and experimental protocols limits the generalizability of existing findings. Nevertheless, H2 appears well-tolerated with few adverse effects. The review identifies standardization of protocols, optimization of dosing regimens, and investigation of long-term outcomes as priority areas for future research.
H2 selectively scavenges reactive oxygen species, suppresses astrocyte and microglial activation, and mitigates mitochondrial dysfunction, thereby reducing neuroinflammation and neuronal damage in sepsis-associated encephalopathy.
This study combines multiple delivery routes. As a general principle, the most efficient route for routine hydrogen intake is inhalation. Inhalation carries explosion risk (empirical LFL of 10%; high-concentration devices are documented in the Consumer Affairs Agency accident database and are not recommended).
See also:
https://h2-papers.org/en/papers/41747800