水素化マグネシウムによるエンドトキシン誘発性急性呼吸窮迫症候群への保護効果：炎症・酸化ストレス・アポトーシス抑制機序の解明
This study examined the effects of magnesium hydride (MgH₂) on lipopolysaccharide (LPS)-induced acute respiratory distress syndrome (ARDS) using A549 alveolar epithelial cells and a murine model. LPS exposure produced oxidative stress, inflammatory cytokine release, apoptosis, and epithelial barrier disruption. MgH₂ administration reduced expression of IL-1β, IL-6, and TNF-α, scavenged intracellular reactive oxygen species, and modulated Bax, Bcl-2, and cytochrome c to limit apoptotic signaling. Barrier integrity was preserved through upregulation of ZO-1 and occludin. Mechanistic analysis revealed decreased phosphorylation of AKT and mTOR, along with reduced NF-κB p65, NLRP3, and cleaved caspase-1 levels, implicating both the AKT/mTOR and NF-κB/NLRP3/IL-1β pathways. In vivo experiments confirmed improved survival rates and attenuated histopathological lung damage in MgH₂-treated mice compared with controls.
MgH₂ downregulates phosphorylated AKT and mTOR while suppressing NF-κB/NLRP3/caspase-1 signaling, thereby reducing LPS-driven cytokine release, ROS accumulation, apoptosis, and alveolar epithelial barrier disruption.
This is basic research at the cellular or molecular level. 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 not recommended).
See also:
https://h2-papers.org/en/papers/35528515