title: Saturated hydrogen saline attenuates endotoxin-induced lung dysfunction.
abstract: BACKGROUND
  Acute lung injury induced by lipopolysaccharides (LPSs) is caused by pulmonary inflammation and pulmonary vascular permeability. Activation of p38 mitogen-activated protein kinase causes inflammation, and proinflammatory cytokines and oxidative stress induce autophagy, a catabolic mechanism responsible for protein degradation and recycling of damaged proteins and cytoplasmic organelles. If not controlled, excessive autophagy responses can result in cell death.
  
  
  METHODS
  In this study, we pretreated rats with saturated hydrogen saline, and examined the molecular mechanism by which saturated hydrogen saline attenuates LPS-induced acute lung dysfunction. Sixty-four male Sprague-Dawley rats were randomly assigned to one of three groups--a control group, an LPS group, or an LPS plus saturated hydrogen saline (LPS + H2) group.
  
  
  RESULTS
  Treatment with saturated hydrogen saline prolonged the median survival time of rats and reduced lung dysfunction induced by LPS. Moreover, saturated hydrogen saline significantly attenuated LPS-mediated induction of serum tumor necrosis factor α, interleukin 6, myeloperoxidase, and malondialdehyde (P < 0.05).
  
  
  CONCLUSIONS
  Autophagosomes were found in the cytoplasm of type II alveolar epithelial cells of LPS-treated rats, and light chain 3 protein (LC3)I/II was increased by LPS treatment. In contrast, saturated hydrogen saline decreased the number of autophagosomes and LC3I/II expression. Saturated hydrogen saline also attenuated the LPS-mediated increase in apoptosis and p38 expression. Taken together, saturated hydrogen saline may attenuate LPS-induced acute lung dysfunction in rats by reducing inflammation, autophagy, and apoptosis involving the p38 mitogen-activated protein kinase signaling pathway.
authors.affiliation: Department of Anesthesiology, Shengjing Affiliated Hospital, China Medical University, Shenyang City, Liaoning Province, PR China.
authors.forename: Yan
authors.initials: Y
authors.lastname: Zhang
authors.affiliation: Department of Anesthesiology, Shengjing Affiliated Hospital, China Medical University, Shenyang City, Liaoning Province, PR China.
authors.forename: Yiming
authors.initials: Y
authors.lastname: Liu
authors.affiliation: Department of Anesthesiology, Shengjing Affiliated Hospital, China Medical University, Shenyang City, Liaoning Province, PR China. Electronic address: zhangj_1@sj-hospital.org.
authors.forename: Jin
authors.initials: J
authors.lastname: Zhang
mesh_terms: D055371:Acute Lung Injury / Q000188:drug therapy* / Q000209:etiology; D000818:Animals; D017209:Apoptosis; D001343:Autophagy; D006859:Hydrogen / Q000627:therapeutic use*; D015227:Lipid Peroxidation; D008070:Lipopolysaccharides / Q000633:toxicity*; D008297:Male; D051381:Rats; D017207:Rats, Sprague-Dawley; D012965:Sodium Chloride / Q000627:therapeutic use*; D048051:p38 Mitogen-Activated Protein Kinases / Q000502:physiology
chemical_list: D008070:Lipopolysaccharides; D012965:Sodium Chloride; D006859:Hydrogen; D048051:p38 Mitogen-Activated Protein Kinases
keywords: Acute lung injury; Apoptosis; Autophagy; Lipopolysaccharide; Saturated hydrogen saline; p38MAPK