急性膵炎モデルにおける水素ガスの保護効果：in vitro・in vivo 統合検討
Acute pancreatitis (AP) involves acinar cell injury and pancreatic inflammation that can escalate into systemic inflammatory responses and multi-organ dysfunction, driven by cytokine–oxidative stress interactions. This study examined the effects of molecular hydrogen (H2) using two complementary models: AR42J cells exposed to cerulein and subsequently cultured in H2-enriched medium for 24 hours (in vitro), and Wistar rats with AP induced by retrograde 5% sodium taurocholate infusion into the pancreatobiliary duct, then exposed to 2% H2 inhalation for 12 hours (in vivo). Measurements included amylase and lipase activity, myeloperoxidase levels, cytokine mRNA expression, 8-hydroxydeoxyguanosine, malondialdehyde, and glutathione concentrations, along with cell viability and histopathological assessment. Both experimental systems showed significant decreases in inflammatory markers and oxidative stress indicators, accompanied by reduced damage to pancreatic tissue and AR42J cells, suggesting H2 gas may serve as a protective agent in AP.
H2 acts as a selective scavenger of hydroxyl radicals and reactive oxygen species, reducing oxidative stress markers (MDA, 8-OHdG) and glutathione depletion, while simultaneously suppressing pro-inflammatory cytokine mRNA expression and myeloperoxidase activity, thereby limiting pancreatic tissue and acinar cell damage.
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/27115738