Hydrogen treatment significantly protects pulmonary epithelial barrier function in septic rats by upregulating aquaporin-1 expression and reducing extravascular lung water accumulation, inflammatory cell infiltration, and alveolar damage. The study demonstrates hydrogen's potential as a therapeutic intervention for sepsis-induced acute lung injury through modulation of water channel proteins and reduction of inflammatory responses. These findings suggest hydrogen therapy may have clinical applications in preventing and treating sepsis-related respiratory complications.
Plain-Language Summary
This study tested whether hydrogen gas could protect lung tissue in rats with sepsis (a severe infection). Researchers gave some rats a bacterial toxin to trigger lung injury, then had them breathe either regular air or 2% hydrogen gas for 6 hours. Rats that breathed hydrogen showed less fluid buildup in their lungs, better oxygen levels, and less inflammatory damage compared to those breathing regular air. The protective effect appeared to work through a protein called aquaporin-1, which helps regulate water movement in lung cells.
Abstract
This study aimed to explore the protective effect of hydrogen and to investigate the underlying mechanism of its preliminary effect on the alveolar epithelial barrier function in septic rats. Forty-five male Sprague-Dawley rats were divided randomly into three groups (N = 15): control [saline injection (intraperitoneal, ip), air drawing; SA], acute lung injury group [lipopolysaccharide (LPS) injection (ip, 15 mg/kg), air drawing; LA], and acute lung injury combined with hydrogen drawing group [LPS injection (ip, 15 mg/kg), 2% hydrogen drawing; LH]. The rats were euthanized after 6 h of treatment, and the extravascular lung water (EVLW), pulmonary alveolar-arterial oxygen pressure (A-aDO2), and respiratory index (RI) of each group were measured. The aquaporin-1 (AQP-1) protein expression in the lung tissues was detected using immunohistochemistry and western blotting, and the correlation between the EVLW and AQP-1 was analyzed. The lung morphology was observed with light and electron microscopy. In the LA group, EVLW (0.87 ± 0.17), A-aDO2 (113.21 ± 13.92), RI (0.65 ± 0.26), and AQP-1 expression increased. Additionally, thickened alveolar walls, significant invasion of inflammatory cells around the vessels, capillary ectasia, hyperemia/hemorrhage in the alveolar space, significantly swollen mitochondria, and increased vacuolar degeneration were observed. A significant negative correlation between AQP-1 expression and EVLW was observed (R2 = 0.8806). Compared with the LA group, EVLW (0.71 ± 0.19), A-aDO2 (132.42 ± 17.39), RI (0.75 ± 0.24), and inflammatory reaction decreased and AQP-1 expression increased in the LH group. The damage to pulmonary epithelial cells improved after hydrogen treatment in rats with sepsis; hydrogen could protect the pulmonary epithelial barrier function by acting on AQP-1.
DOI: 10.4238/gmr.15016050
