妊娠中の水素投与が母体免疫活性化モデルにおける仔マウスの行動異常を改善する
This study examined the long-term neurodevelopmental consequences in offspring using a lipopolysaccharide (LPS)-induced maternal immune activation (MIA) mouse model, and assessed whether maternal H2 administration could mitigate these effects. Offspring born to LPS-exposed dams exhibited impaired short-term memory and reduced social interaction, accompanied by neuronal and oligodendrocytic loss in the amygdala and cortex, as evaluated by Y-maze, three-chamber, and prepulse inhibition tests at postnatal weeks 3–4, and immunohistochemistry at week 5. Maternal H2 administration substantially reduced these LPS-induced behavioral and histological abnormalities. Additionally, the number of hypertrophic activated astrocytes was elevated in LPS-exposed offspring but diminished when dams received H2. In primary astrocyte cultures, H2 suppressed LPS-induced pro-inflammatory cytokine production. These findings collectively suggest that maternal H2 administration confers neuroprotective effects and reduces MIA-associated neurodevelopmental deficits in offspring.
H2 scavenges reactive oxygen species, thereby suppressing neuroinflammatory cascades including microglial activation, pro-inflammatory cytokine induction, and astrocyte hypertrophy, which collectively protect fetal neurons and oligodendrocytes from LPS-induced damage.
This study is at the animal-experiment stage. For human application, inhalation is the most promising delivery route, but inhalation carries explosion risk and concentration matters (empirical LFL of 10%; high-concentration devices are documented in the Consumer Affairs Agency accident database and are not recommended).
See also:
https://h2-papers.org/en/papers/29907804