敗血症関連脳症ラットモデルにおける水素富化生理食塩水の神経炎症およびミトコンドリア機能障害への影響
Sepsis-associated encephalopathy (SAE) is a form of organ dysfunction lacking overt central nervous system infection, carrying substantial mortality and long-term neurological consequences. Using a juvenile rat model in which sepsis was induced by intraperitoneal lipopolysaccharide (LPS, 8 mg/kg), hydrogen-rich saline (HRS, 5 ml/kg) was administered 1 hour post-induction. At 48 hours, HRS-treated animals showed improved survival and reduced neuronal injury on Nissl staining. ELISA revealed lower TNF-α and IL-1β alongside elevated IL-10. TUNEL assay demonstrated fewer apoptotic cells, and immunohistochemistry showed diminished GFAP and IBA-1 immunoreactivity, indicating suppressed astrocyte and microglial activation. Mitochondrial membrane potential (JC-1) and ATP content, both reduced by LPS, were restored by HRS, while LPS-elevated ROS levels declined. Transmission electron microscopy confirmed increased mitochondrial and synaptic counts and improved ultrastructural integrity in HRS-treated rats. Collectively, these findings indicate that HRS mitigates neuroinflammation, glial activation, apoptosis, and mitochondrial dysfunction in juvenile SAE.
HRS suppresses neuroinflammation by reducing TNF-α and IL-1β while elevating IL-10, and protects mitochondrial function by restoring membrane potential and ATP production while decreasing ROS generation, thereby limiting apoptosis and glial activation.
Intravenous hydrogen-saline infusion is a clinic-only route and is not viable for everyday self-administration. For routine hydrogen intake, inhalation is the most practical route, but inhalation carries explosion risk and concentration matters (empirical LFL of 10%; high-concentration 66% / 100% devices are not recommended).
See also:
https://h2-papers.org/en/papers/36435787