慢性炎症におけるTLR4ラジカルサイクルの役割と分子状水素を含む介入候補のレビュー
Toll-like receptor 4 (TLR4), a component of innate immunity, has been implicated in the pathophysiology of a broad spectrum of conditions including asthma, cardiovascular disease, diabetes, obesity, autoimmune disorders, neuroinflammatory conditions, schizophrenia, bipolar disorder, autism, depression, and chronic fatigue syndrome. Environmental triggers such as ozone, atmospheric particulate matter, lipopolysaccharide (LPS) from gram-negative bacteria, ionizing radiation, and toluene can activate TLR4 signaling, leading to elevated reactive oxygen and nitrogen species (ROS/RNS) and sustained oxidative-nitrosative stress. This review examines agents capable of attenuating TLR4-mediated inflammatory cascades, including anti-LPS peptides, recombinant factor C, TLR4/MyD88 antagonists such as eritoran, epigallocatechin-3-gallate, 6-shogaol, N-acetylcysteine, melatonin, and molecular hydrogen. The authors propose that a TLR-driven ROS/RNS cycle represents a shared mechanistic pathway across numerous chronic inflammatory conditions, and that modulating this cycle may offer broad benefit.
TLR4 activation drives ROS/RNS overproduction, sustaining a radical cycle that perpetuates chronic inflammation. Molecular hydrogen is identified as a candidate agent capable of interrupting this TLR4-mediated oxidative-nitrosative cascade.
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/23436141