Treatment with exogenous hydrogen sulfide attenuates hyperoxia-induced acute lung injury in mice

The aim of this work was to test the effect of treatment with hydrogen sulfide (H 2 S) on hyperoxia-induced acute lung injury in mice. Mice were exposed to room air or 95 % O 2 , and treated with NaHS (intraperitoneal injection of 0.1 ml/kg/day of 0.56 mol/l NaHS). Treatment with H 2 S partly restored the reduced H 2 S levels in plasma and lungs of mice exposed to hyperoxia. Treatment with H 2 S attenuated hyperoxia-induced acute lung injury marked by reduced ratio of lung weight to body weight, ratio of lung wet weight to dry weight, and cell numbers and protein content in bronchoalveolar lavage (BAL) and decreased apoptosis. Treatment with H 2 S markedly prolonged the survival of mice under oxygen exposure. Treatment with H 2 S abated hyperoxia-induced oxidative stress marked by reduced malondialdehyde and peroxynitrite formation, reduced NADPH oxidase activity, enhanced translocation of nuclear factor E2-related factor (Nrf2) into nucleus and increased activity of HO-1. Treatment with H 2 S decreased IL-1β, MCP-1, and MIP-2, and increased IL-10 expression in lungs of mice exposed to hyperoxia. Treatment with H 2 S decreased NFκB activity and iNOS expression in lungs, and reduced NOx content in BAL of mice exposed to hyperoxia. Treatment with H 2 S reduced lung permeability and suppressed VEGF release and VEGFR2 expression in lungs of mice under oxygen exposure. Treatment with exogenous H 2 S attenuated hyperoxia-induced acute lung injury through abating oxidative stress, suppressing inflammation, and reducing lung permeability in mice.