脊髄損傷ラットにおける分子状水素による酸化傷害関連反応性アストログリオーシスの抑制
This study examined whether molecular hydrogen could reduce excessive astrocyte activation following spinal cord injury (SCI) in rats and in H2O2-challenged cultured astrocytes. Hydrogen-rich saline (8 mL/kg, i.p.) was administered every 12 hours post-SCI. By postoperative day 3, STAT3, phosphorylated STAT3, and GFAP expression were reduced alongside decreased levels of IL-1β, IL-6, and TNF-α in the injured spinal cord. On days 7 and 14, reactive astrogliosis was attenuated and locomotor function improved. In cultured astrocytes exposed to H2O2, hydrogen-rich medium reduced intracellular ROS production—particularly hydroxyl radicals—and diminished proinflammatory cytokine secretion. These findings suggest that molecular hydrogen exerts neuroprotective effects by suppressing oxidative stress-driven astrogliosis and associated neuroinflammation after contusive SCI.
Molecular hydrogen selectively scavenges hydroxyl radicals, thereby suppressing STAT3 phosphorylation in astrocytes, which reduces GFAP upregulation, reactive astrogliosis, and the release of proinflammatory cytokines including IL-1β, IL-6, and TNF-α.
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/24685114