サンゴカルシウム水素化物によるARDS急性肺傷害の軽減：Trx2/Myo19/Drp1経路を介したミトコンドリア末梢分裂の促進
This study investigated the effects of coral calcium hydride (CCH), a solid-form molecular hydrogen carrier derived from coral calcium, on lipopolysaccharide (LPS)-induced acute lung injury in a mouse model of acute respiratory distress syndrome (ARDS). Survival rates in CCH-treated mice were comparable to those receiving hydrogen gas inhalation, both significantly exceeding the untreated ARDS group. CCH administration reduced pulmonary hemorrhage and edema while improving lung function and local microcirculation. Mechanistically, CCH activated mitochondrial thioredoxin 2 (Trx2), which promoted peripheral mitochondrial fission via the Myo19/Drp1 axis during early ARDS progression. This action corrected LPS-induced mitochondrial dysfunction and diminished oxidative stress damage in alveolar type-II (AT-II) cells. The findings suggest CCH functions as an efficient hydrogen-releasing agent capable of mitigating ARDS-associated acute lung injury through restoration of mitochondrial quality control.
CCH activates mitochondrial thioredoxin 2 (Trx2), which in turn promotes peripheral mitochondrial fission through the Myo19/Drp1 pathway, thereby correcting LPS-induced mitochondrial dysfunction and reducing oxidative stress in AT-II cells.
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/40177064