title: Protective effect and mechanism of hydrogen treatment on lung epithelial barrier dysfunction in rats with sepsis.
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.
authors.affiliation: Shengjing Hospital of China Medical University, Shenyang, Liaoning Province, China.
authors.forename: L-D
authors.initials: LD
authors.lastname: Liu
authors.affiliation: Shengjing Hospital of China Medical University, Shenyang, Liaoning Province, China.
authors.forename: X-Y
authors.initials: XY
authors.lastname: Wu
authors.affiliation: Shengjing Hospital of China Medical University, Shenyang, Liaoning Province, China.
authors.forename: B-D
authors.initials: BD
authors.lastname: Tao
authors.affiliation: Shengjing Hospital of China Medical University, Shenyang, Liaoning Province, China.
authors.forename: N
authors.initials: N
authors.lastname: Wang
authors.affiliation: Shengjing Hospital of China Medical University, Shenyang, Liaoning Province, China.
authors.forename: J
authors.initials: J
authors.lastname: Zhang
mesh_terms: D055371:Acute Lung Injury / Q000188:drug therapy* / Q000209:etiology / Q000378:metabolism / Q000473:pathology; D000818:Animals; D051398:Aquaporin 1 / Q000187:drug effects* / Q000235:genetics; D004847:Epithelial Cells / Q000187:drug effects* / Q000378:metabolism; D005786:Gene Expression Regulation; D006859:Hydrogen / Q000494:pharmacology* / Q000627:therapeutic use; D008297:Male; D020011:Protective Agents / Q000494:pharmacology; D011650:Pulmonary Alveoli / Q000187:drug effects* / Q000378:metabolism / Q000473:pathology; D051381:Rats; D017207:Rats, Sprague-Dawley; D018805:Sepsis / Q000150:complications*
chemical_list: C496022:Aqp1 protein, rat; D020011:Protective Agents; D051398:Aquaporin 1; D006859:Hydrogen