Abstract

Objective To evaluate the effect of exogenous hydrogen sulfide on phenotypic transformation of alveolar macrophages in a mouse model of endotoxin-induced acute lung injury (ALI). Methods Thirty pathogen-free healthy male C57BL/6 mice, aged 8 weeks, weighing 18-20 g, were divided into 3 groups (n=10 each) using a random number table: sham operation group (group Sham), group ALI and exogenous hydrogen sulfide group (group NaHS). In group Sham, normal saline was intratracheally instilled and intraperitoneally injected.In ALI and NaHS groups, lipopolysaccharide 20 mg/kg was intratracheally instilled, and normal saline and sodium hydrosulfide (28 μmol/kg) 100 μl were intraperitoneally injected, respectively, every day.Mice were sacrificed at day 3 after administration of lipopolysaccharide, and lungs were removed for measurement of the lung coefficient and expression of inducible nitric oxide synthase (iNOS) and arginase (by immunohistochemistry) and for microscopic examination of the pathological changes.Lung injury was evaluated by the index of quantitative assessment (IQA). Results Compared with group Sham, the lung coefficient and IQA were significantly increased, and the expression of iNOS and arginase in lung tissues was up-regulated in group ALI (P 0.05). Conclusion Exogenous hydrogen sulfide mitigates endotoxin-induced ALI through inhibiting phenotypic transformation of alveolar macrophages to M1 subtype in mice. Key words: Hydrogen sulfide; Respiratory distress syndrome, adult; Endotoxins; Macrophages; Phenotype

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