Abstract

The aim of this study was to investigate the efficacy and underlying mechanism of high concentration of hydrogen on lipopolysaccharide (LPS)-induced acute lung injury (ALI). We have established a corresponding mouse model and examined the function of hydrogen inhalation on lung pathology and pulmonary edema induced by LPS, as well as contents of IL-1β, TNF-α and IL-8. The pulmonary microvascular permeability and 66.7% hydrogen on the expression of sirt1 and its downstream signaling molecules were tested. Results showed that 66.7% hydrogen alleviated lung pathological changes and pulmonary edema caused by LPS, and reduced the degree of ALI by inhibiting pro-inflammatory cytokine release and oxidative stress response, thereby decreasing the expression of molecules related to intercellular adhesion. sirt1 contributed to the repair of LPS-induced ALI by hydrogen through the regulation of NF-κB and catalase expression. In conclusion, 66.7% hydrogen protected against LPS-induced ALI by suppressing inflammatory response and oxidative stress mediated by NF-κB and catalase in a sirt1-dependent manner.