母体への水素投与がLPS誘発胎仔肺障害を軽減する：ラットモデルおよびヒト肺上皮細胞を用いた検討
Maternal inflammation is a recognized risk factor for preterm birth and neonatal respiratory complications. This study examined whether molecular hydrogen (H2) could reduce fetal lung injury triggered by lipopolysaccharide (LPS)-induced maternal inflammation. In A549 human lung epithelial cells, H2-rich medium significantly suppressed LPS-induced increases in reactive oxygen species (ROS), interleukin-6 (IL-6), and apoptotic cell counts. In pregnant Sprague-Dawley rats, H2-rich water was provided ad libitum for 24 hours prior to intraperitoneal LPS injection on gestational day 19. Fetal lung tissue collected on day 20 showed significantly elevated cleaved caspase-3, 8-hydroxy-2'-deoxyguanosine (8-OHdG), IL-6, and vascular endothelial growth factor (VEGF) in the LPS group; all markers were significantly reduced in the H2 water plus LPS group. These findings indicate that maternal H2 intake attenuates oxidative damage, apoptosis, and inflammatory signaling in fetal lung tissue, suggesting a potential role for antenatal H2 administration in reducing inflammation-associated pulmonary morbidity in premature infants.
H2 suppresses LPS-induced ROS generation and IL-6-mediated inflammatory signaling, thereby reducing caspase-3-dependent apoptosis and oxidative DNA damage (8-OHdG) in fetal lung cells. VEGF dysregulation associated with inflammation was also attenuated.
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/25947958