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Recent Advances in Studies of Molecular Hydrogen against Sepsis.

敗血症に対する水素分子の研究における最近の進展

review not specified not assessed

Abstract

Sepsis is a life-threatening syndrome arising from a dysregulated host response to infection, leading to multi-organ dysfunction. Molecular hydrogen has attracted attention as a novel antioxidant capable of scavenging free radicals, with documented efficacy across conditions including infection, trauma, ischemia-reperfusion injury, metabolic disorders, and malignancies. This review examines the biological actions of molecular hydrogen relevant to sepsis, encompassing anti-inflammatory, antioxidative, anti-apoptotic, anti-shock, and autophagy-regulatory effects, all of which may reduce organ and barrier damage associated with sepsis. The current state of knowledge regarding underlying signaling pathways is discussed, and the review aims to provide a mechanistic framework for future investigation into hydrogen's role in sepsis management.

Mechanism

Molecular hydrogen is proposed to mitigate sepsis-induced organ and barrier injury by scavenging reactive oxygen species, suppressing inflammatory signaling cascades, and modulating apoptotic and autophagic pathways.

Bibliographic

Authors
Qiu P, Liu Y, Zhang JH
Journal
Int J Biol Sci
Year
2019
PMID
31223285
DOI
10.7150/ijbs.30741
PMC
PMC6567800

Tags

Disease:虚血再灌流障害 敗血症 Mechanism:アポトーシス抑制 オートファジー 炎症抑制 酸化ストレス 活性酸素種

Delivery context

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).

Safety notes

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:

Other papers on the same disease / condition

Cite as: H2 Papers — PMID 31223285. https://h2-papers.org/en/papers/31223285
Source: PubMed PMID 31223285