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Perspective of Molecular Hydrogen in the Treatment of Sepsis.

敗血症に対する分子状水素の効果:メカニズムと臨床応用の展望

review mixed routes not assessed

Abstract

Sepsis remains a leading cause of mortality among critically ill patients, characterized by life-threatening multi-organ dysfunction arising from a dysregulated host response to infection. This review examines the biological effects of molecular hydrogen (H2) gas on sepsis-associated organ damage. H2 has been reported to exert multiple protective actions, including suppression of inflammatory cascades, reduction of oxidative stress, inhibition of apoptotic pathways, modulation of autophagy, and interaction with various intracellular signaling networks. The review synthesizes current mechanistic evidence and discusses the theoretical foundation for future clinical use of H2 in sepsis management.

Mechanism

H2 is proposed to mitigate sepsis-induced multi-organ injury by suppressing inflammatory mediators, reducing oxidative damage, inhibiting apoptosis, regulating autophagy, and modulating multiple intracellular signaling pathways.

Bibliographic

Authors
Qi B, Wang Y, Yu Y, Xie K
Journal
Curr Pharm Des
Year
2021
PMID
32912119
DOI
10.2174/1381612826666200909124936

Tags

Disease:敗血症 Mechanism:アポトーシス抑制 オートファジー 炎症抑制 ミトコンドリア 酸化ストレス 活性酸素種

Delivery context

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).

Safety notes

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:

Other papers on the same disease / condition

Cite as: H2 Papers — PMID 32912119. https://h2-papers.org/en/papers/32912119
Source: PubMed PMID 32912119