a Department of Anesthesiology, Nanjing First Hospital, Nanjing Medical University, Jiangsu, 210000, China;
b Department of Anesthesiology, Jiangning Hospital Affiliated to Nanjing Medical University, Nanjing, 211100, China;
c Department of Anesthesiology, Nanjing Hospital of Chinese Medicine affiliated to Nanjing University of Chinese Medicine, Nanjing, Jiangsu 211100, China;
d Department of Anesthesiology, the First Affiliated Hospital of Naval Medical University, Shanghai 200433, China;
e Jinling College affiliated to Nanjing Medical University, Nanjing, Jiangsu 211100, China;
f Wuxi Taihu University, Wuxi, Jiangsu 214064, China;
g Department of Anesthesiology, BenQ Medical Center, The Affiliated BenQ Hospital of Nanjing Medical University, Nanjing, 210019, China;
h Jiangsu Key Laboratory of Neurodegeneration, Department of Pharmacology, Nanjing Medical University, Nanjing, Jiangsu 211166, China
Funds:
This work was supported by Nanjing Medical Science and Technology Development Project (YKK23221)
Open Project of Immune Cell Translational Research Center of Jiangning Hospital, Nanjing Medical University (JNYYZXKY202216)
General Project of Medical Education Collaborative Innovation Fund of Jiangsu University (JDYY2023094)
China Red Cross Foundation Medical empowerment charity special fund project (CRCF-YXFN-202302028).
Acute respiratory distress syndrome (ARDS) is a common respiratory emergency, but current clinical treatment remains at the level of symptomatic support and there is a lack of effective targeted treatment measures. Our previous study confirmed that inhalation of hydrogen gas can reduce the acute lung injury of ARDS, but the application of hydrogen has flammable and explosive safety concerns. Drinking hydrogen-rich liquid or inhaling hydrogen gas has been shown to play an important role in scavenging reactive oxygen species and maintaining mitochondrial quality control balance, thus improving ARDS in patients and animal models. Coral calcium hydrogenation (CCH) is a new solid molecular hydrogen carrier prepared from coral calcium (CC). Whether and how CCH affects acute lung injury in ARDS remains unstudied. In this study, we observed the therapeutic effect of CCH on lipopolysaccharide (LPS) induced acute lung injury in ARDS mice. The survival rate of mice treated with CCH and hydrogen inhalation was found to be comparable, demonstrating a significant improvement compared to the untreated ARDS model group. CCH treatment significantly reduced pulmonary hemorrhage and edema, and improved pulmonary function and local microcirculation in ARDS mice. CCH promoted mitochondrial peripheral division in the early course of ARDS by activating mitochondrial thioredoxin 2(Trx2), improved lung mitochondrial dysfunction induced by LPS, and reduced oxidative stress damage. The results indicate that CCH is a highly efficient hydrogen-rich agent that can attenuate acute lung injury of ARDS by improving the mitochondrial function through Trx2 activation.