水素富化生理食塩水によるモルモット網膜グルタミン酸興奮毒性傷害への保護効果
A guinea pig model of retinal excitotoxicity was established by intravitreal glutamate injection to evaluate the neuroprotective potential of hydrogen-rich saline. Administration of hydrogen-rich saline via intravitreal, intraperitoneal, or combined routes 30 minutes after injury was assessed at 7 days. Combined delivery produced the greatest preservation of retinal ganglion cell (RGC) layer cellularity and overall retinal thickness, along with reduced ultrastructural damage. Glial activation markers—GFAP in Müller cells, CD11b in microglia, and iNOS and GRP78 in glial cells—were all downregulated. Concurrently, expression of the glutamate transporter EAAT-1 was elevated, suggesting improved glutamate clearance. These findings indicate that hydrogen-rich saline mitigates glutamate-mediated retinal damage through suppression of glial activation and restoration of excitatory amino acid transport.
Hydrogen-rich saline suppresses glial cell activation, reduces iNOS and GRP78 expression, and upregulates the glutamate transporter EAAT-1, thereby enhancing glutamate clearance and attenuating excitotoxic retinal damage via antioxidant and anti-inflammatory pathways.
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).
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https://h2-papers.org/en/papers/22154552