水素分子による骨芽細胞のTNFα誘発性細胞障害に対する保護効果
TNFα is a key mediator in inflammatory conditions including rheumatoid arthritis and postmenopausal osteoporosis. Using osteoblasts isolated from neonatal rat calvariae, this study examined how molecular hydrogen (H2) affects TNFα-induced cellular damage. TNFα reduced cell viability, promoted apoptosis, downregulated Runx2 mRNA, and diminished alkaline phosphatase activity; co-incubation with H2 reversed all these changes. H2 also counteracted TNFα-driven increases in intracellular ROS, malondialdehyde, and NADPH oxidase activity. Mitochondrial dysfunction—evidenced by elevated mitochondrial ROS, reduced membrane potential, and decreased ATP synthesis—was similarly attenuated. Activities of antioxidant enzymes SOD and catalase were restored. H2 suppressed TNFα-induced NF-κB pathway activation, inhibited iNOS-mediated nitric oxide production, and reduced IL-6 and ICAM-1 mRNA expression. Collectively, these findings indicate that H2 protects osteoblasts from TNFα-induced injury by reducing oxidative stress, preserving mitochondrial integrity, dampening inflammatory signaling, and improving NO bioavailability.
H2 suppresses NF-κB pathway activation and NADPH oxidase-derived ROS generation, restores SOD and catalase activities, preserves mitochondrial membrane potential and ATP synthesis, and inhibits iNOS-mediated nitric oxide overproduction, collectively reducing oxidative and inflammatory damage in osteoblasts.
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/23212446