水素による血管平滑筋細胞の増殖・遊走抑制：MAPKおよびERM経路の下方制御を介したメカニズム解析
This study examined how molecular hydrogen affects angiotensin II (Ang II)-driven proliferation and migration of vascular smooth muscle cells (VSMCs) in vitro, and abdominal aortic coarctation (AAC)-induced vascular hypertrophy in vivo. Hydrogen-rich medium (0.6–0.9 ppm) was applied 30 minutes before 10⁻⁷ M Ang II, with endpoints assessed at 24 hours. In the animal model, pure hydrogen gas (99.999%) was administered intraperitoneally at 1 ml/100 g/day for one week prior to AAC and continued for six weeks. Hydrogen reduced reactive oxygen species in Ang II-stimulated VSMCs, lowered 3-nitrotyrosine in vascular tissue, and decreased serum malondialdehyde. Phosphorylation of ERK1/2, p38 MAPK, JNK, and ezrin/radixin/moesin (ERM) proteins was also suppressed. These findings suggest that ROS-dependent MAPK and ERM signaling mediates the inhibitory effects of hydrogen on VSMC proliferation, migration, and vascular remodeling.
Hydrogen scavenges reactive oxygen species, thereby suppressing phosphorylation of ERK1/2, p38 MAPK, JNK, and ERM proteins, which reduces Ang II-induced VSMC proliferation and migration as well as AAC-induced vascular hypertrophy.
This study combines multiple delivery routes. As a general principle, the most efficient route for routine hydrogen intake is inhalation. Inhalation carries explosion risk (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/26875562