High concentration of hydrogen ameliorates lipopolysaccharide-induced acute lung injury in a sirt1-dependent manner

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-1 beta, TNF-alpha 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 LPSinduced ALI by hydrogen through the regulation of NF-kappa B and catalase expression. In conclusion, 66.7 % hydrogen protected against LPS-induced ALI by suppressing inflammatory response and oxidative stress mediated by NF-kappa B and catalase in a sirt1-dependent manner.