敗血症関連脳症における病態機序：ミトコンドリア機能障害と神経炎症の相互作用および新興介入戦略のレビュー
Sepsis-associated encephalopathy (SAE) is a severe neurological complication characterized by diffuse brain dysfunction, persistent cognitive impairment, and elevated mortality. This review examines the bidirectional pathogenic relationship between mitochondrial dysfunction and neuroinflammation in SAE. Key mitochondrial disturbances include Drp1-driven fission, impaired biogenesis through the PGC-1α axis, oxidative stress accumulation, and activation of cell death programs such as ferroptosis and pyroptosis. Microglial activation mediated by the NLRP3 inflammasome amplifies mitochondrial damage and synaptic deterioration, forming a self-reinforcing cycle. The review also surveys emerging strategies targeting this axis, among which molecular hydrogen is highlighted alongside mitochondria-targeted peptides, natural compounds, and specific molecular inhibitors. Insights from gut-brain axis research and cerebral metabolomics are noted as expanding the mechanistic and interventional landscape for improving neurological outcomes in septic patients.
Molecular hydrogen is proposed to interrupt the self-amplifying cycle of mitochondrial dysfunction and neuroinflammation in SAE, potentially by suppressing NLRP3 inflammasome activation and reducing oxidative stress burden in neuronal tissue.
The delivery route is not clearly identifiable from this paper. For hydrogen intake, inhalation is the most efficient route; inhalation, however, carries explosion risk (empirical LFL of 10%; high-concentration devices are not recommended).
See also:
https://h2-papers.org/en/papers/42057900