水素豊富生理食塩水による頸動脈バルーン傷害後の新生内膜形成抑制：ROSおよびTNF-α/NF-κB経路の関与
This study examined the effects of daily hydrogen-rich saline solution (HRSS) injection in a rat carotid balloon-injury model. Animals receiving HRSS showed a significant reduction in neointima area and intima-to-media ratio, along with fewer PCNA-positive proliferating cells in the intimal layer. In the injured carotid arteries, ROS and malondialdehyde (MDA) levels declined, while superoxide dismutase (SOD) activity and reduced glutathione (GSH) concentrations increased. Inflammatory mediators including IL-6, TNF-α, and NF-κB p65 were also markedly reduced. Complementary cell-culture experiments demonstrated that hydrogen solution inhibited PDGF-BB-induced vascular smooth muscle cell (VSMC) proliferation and attenuated ROS generation. Collectively, the findings indicate that HRSS may limit post-angioplasty restenosis partly by scavenging local ROS and downregulating the TNF-α/NF-κB signaling axis.
HRSS scavenges local reactive oxygen species and suppresses the TNF-α/NF-κB signaling pathway, thereby reducing vascular smooth muscle cell proliferation and inflammatory cytokine production to limit neointima formation after arterial injury.
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/22153150