水素水の長期摂取がLPS誘発慢性肝障害ラットにおける酸化ストレス・肝炎症・アポトーシスを軽減する
Chronic hepatic inflammation underlies the progression of various metabolic liver diseases, yet the long-term effects of hydrogen-rich water (HRW) on this condition had not been well characterized. Sprague-Dawley rats received HRW for 8 months before and during exposure to lipopolysaccharide (LPS) to establish a chronic liver injury model. Sustained HRW administration suppressed inflammatory cell infiltration in hepatic tissue, blunted abnormal rises in pro-inflammatory mediators, and stabilized anti-inflammatory factor expression. Apoptotic signaling through the death receptor, mitochondrial, and endoplasmic reticulum stress pathways—reflected by Bax, cytochrome c, Caspase-3, -8, -9, -12, CHOP, and GRP78—was attenuated, while the anti-apoptotic protein Bcl-2 was preserved. These findings indicate that long-term HRW consumption may delay chronic inflammation-driven liver injury by concurrently reducing oxidative stress, mitochondrial dysfunction, and apoptotic activity.
HRW suppresses pro-apoptotic signaling via the death receptor, mitochondrial, and ER stress pathways—downregulating Bax, Caspase-3/-8/-9/-12, CHOP, and GRP78—while maintaining Bcl-2 expression, thereby reducing hepatocyte apoptosis and oxidative stress-driven liver injury.
Hydrogen-rich water is a low-risk delivery route, but the achievable systemic hydrogen dose is bounded. For clinical applications, inhalation is the most efficient route; inhalation, however, carries explosion risk, and concentration matters (empirical LFL of 10% applies to inhalation environments; high-concentration devices are documented in the Consumer Affairs Agency accident database and are not recommended).
See also:
https://h2-papers.org/en/papers/41750640