Abstract: ［Abstract］ Objective〖HTSS〗To investigate the effect of high concentration of hydrogen-rich saline on acute lung injury induced by intraperitoneal injection of lipopolysaccharide(LPS).
  〖WTHZ〗Methods〖HTSS〗Sixty male SD rats of clean grade were randomly divided into blank group hydrogen-rich saline group, LPS group and LPS + hydrogen-rich saline group, with 15 rats in each group. LPS group and LPS + hydrogen-rich saline group were injected intraperitoneally with LPS 10 mg/kg to establish sepsis model in rats. hydrogen-rich salin group and LPS + hydrogen-rich saline group were intraperitoneally injected with 5 mL/kg high concentration high concentration hydrogen-rich saline immediately, 3 h, 6 h, 12 h and 18 h after operation. Blank group and LPS 〖JP2〗group were given intraperitoneal injection of normal saline. Bronchoalveolar lavage fluid was used to detect neutrophil count, malondialdehyde(MDA)content, superoxide dismutase(SOD), myeloperoxidase〖JP〗(MPO), glutathione peroxidase(GSH-Px) activity in lung tissue, and Western blot was used to detect the expression of nuclear factor erythroid-2-related factor-2(Nrf2) and hemeoxygenase-1(HO-1)in lung tissue.
  〖WTHZ〗Results〖HTSS〗Compared with LPS group, the mean survival time of rats in LPS + hydrogen-rich salin group was prolonged in 7 days(P＜0.05). Compared with blank group, the number of neutrophils and the content of MDA in LPS group were significantly increased, the activities of SOD, MPO and GSH-Px were decreased(P＜0.05), and the expressions of Nrf2 and HO-1 in lung tissue were increased(P＜0.05). Compared with LPS group, the expression of Nrf2 and HO-1 in lung tissue was increased(P＜0.05). In hydrogen-rich salin group, neutrophil count, MDA content was decreased, SOD, MPO, GSH-Px activity, Nrf2 and HO-1 expression were increased significantly(P＜0.05).
  〖WTHZ〗Conclusion〖HTSS〗High concentration hydrogen-rich saline can prolong the mean survival time of LPS-induced sepsis rats, reduce inflammatory cells and oxidative stress in the lung, and may control acute lung injury through Nrf2/HO-1 pathway.

Key words: sepsis, acute lung injury, lipopolysaccharides, rats