水素富化生理食塩水による光誘発性網膜障害保護におけるSirtuin 1の媒介機序
In a rat model of intense light-induced retinal injury, intraperitoneal administration of hydrogen-rich saline (HRS) for 5 days elevated Sirt1 (Sirtuin Type 1) expression, partially preserved electroretinogram a- and b-wave amplitudes, and reduced outer nuclear layer cell loss. The Sirt1 activator resveratrol reproduced these protective outcomes, while the Sirt1 inhibitor EX-527 and Sirt1-targeting siRNAs each abolished the benefits of HRS, confirming Sirt1 as a necessary mediator. HRS also upregulated Bcl-2 protein and superoxide dismutase activity, and in a Sirt1-dependent fashion reduced Bax expression, cleaved caspase-3 levels, and the lipid peroxidation marker malondialdehyde. Collectively, these findings indicate that HRS confers retinal protection against phototoxic injury primarily through Sirt1-mediated suppression of apoptosis and oxidative stress.
HRS upregulates Sirt1, which in turn promotes Bcl-2 expression, suppresses Bax and cleaved caspase-3 to inhibit apoptosis, and enhances SOD activity while reducing malondialdehyde, collectively protecting retinal cells from phototoxic oxidative damage.
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/26720481