title: [Protective effects of inhaled hydrogen gas on cognitive function in mice with sepsis-associated encephalopathy].
abstract: OBJECTIVE
  To evaluate protective effects of inhaled hydrogen gas (H2) on cognitive function in a murine model of sepsis-associated encephalopathy (SAE).
  
  
  METHODS
  A total of 84 male ICR mice, weighing 20-25 g, aged 6-8 weeks, were randomly divided into 4 groups of sham, sham+H2, sepsis and sepsis+H2. Sepsis was established by cecal ligation and puncture (CLP). Mice in sham+H2 and sepsis+H2 groups received 2% H2 inhalation for 1 h at 1 h and 6 h after sham operation or CLP operation respectively. The changes of neurological function and neuronal damage in hippocampal CA1 region were observed at 24 h post-operation. The activities of superoxide dismutase (SOD) and catalase (CAT) and the levels of malondialdehyde (MDA) and 8-iso-prostaglandin F2α (8-iso-PGF2α) in sera and hippocampus were detected at 24 h post-operation. The changes of cognitive function were observed by Y-maze test and fear conditional test at days 3 to 14 post-operation.
  
  
  RESULTS
  Compared with sham group, the neurological function significantly declined and neurons in hippocampal CA1 region were significantly damaged; the activities of SOD and CAT markedly decreased while the levels of MDA and 8-iso-PGF2α markedly increased in sera and hippocampus; the time in new zone and the percentage of freezing time dramatically decreased at days 3 to 14 post-operation in sepsis group (P < 0.05) . Compared with sepsis group, neurological function significantly improved and damaged neurons in hippocampal CA1 region significantly reduced; the activities of SOD and CAT markedly increased and the levels of MDA and 8-iso-PGF2α markedly decreased in sera and hippocampus; the time in new zone and the percentage of freezing time dramatically increased at days 3 to 14 post-operations in sepsis+H2 group (P < 0.05).
  
  
  CONCLUSIONS
  H2 inhalation can significantly alleviate neuronal damage and improve cognitive dysfunction in CLP-induced SAE mice. And it is probably associated with the increased activities of antioxidant enzymes and the reduced levels of oxidative products.
authors.affiliation: Department of Anesthesiology, Tianjin Medical University General Hospital, Tianjin Institute of Anesthesiology, Tianjin 300052, China.
authors.forename: Lingling
authors.initials: L
authors.lastname: Liu
authors.affiliation: Department of Anesthesiology, Tianjin Medical University General Hospital, Tianjin Institute of Anesthesiology, Tianjin 300052, China.
authors.forename: Keliang
authors.initials: K
authors.lastname: Xie
authors.affiliation: Department of Anesthesiology, Tianjin Medical University General Hospital, Tianjin Institute of Anesthesiology, Tianjin 300052, China.
authors.forename: Hongguang
authors.initials: H
authors.lastname: Chen
authors.affiliation: Department of Anesthesiology, Tianjin Medical University General Hospital, Tianjin Institute of Anesthesiology, Tianjin 300052, China.
authors.forename: Xiaoqing
authors.initials: X
authors.lastname: Dong
authors.affiliation: Department of Anesthesiology, Tianjin Medical University General Hospital, Tianjin Institute of Anesthesiology, Tianjin 300052, China.
authors.forename: Yuan
authors.initials: Y
authors.lastname: Li
authors.affiliation: Department of Anesthesiology, Tianjin Medical University General Hospital, Tianjin Institute of Anesthesiology, Tianjin 300052, China. Email: yuyonghao@126.com.
authors.forename: Yonghao
authors.initials: Y
authors.lastname: Yu
mesh_terms: D000818:Animals; D003071:Cognition; D003072:Cognition Disorders; D015237:Dinoprost / Q000031:analogs & derivatives; D004195:Disease Models, Animal; D006624:Hippocampus; D006859:Hydrogen; D008297:Male; D008315:Malondialdehyde; D051379:Mice; D008813:Mice, Inbred ICR; D009474:Neurons; D065166:Sepsis-Associated Encephalopathy; D013482:Superoxide Dismutase
chemical_list: C075750:8-epi-prostaglandin F2alpha; D008315:Malondialdehyde; D006859:Hydrogen; D015237:Dinoprost; D013482:Superoxide Dismutase