title: Glabridin attenuates lipopolysaccharide-induced acute lung injury by inhibiting p38MAPK/ERK signaling pathway.
abstract: BACKGROUND
  Acute respiratory distress syndrome (ARDS) is a complication caused by pulmonary and/or external factors. In this study, we investigated the protective mechanisms of glabridin in lipopolysaccharide (LPS) induced ARDS in rats.
  
  
  RESULTS
  GLA treatment at dose of 30 mg/kg decreased LPS-induced lung W/D ratio and alleviated evident lung histopathological changes. Expressions of TNF-α and IL-18 were suppressed by GLA in plasma. The levels of SPA, MDA and NO in lung were down-regulated significantly in groups administrated with GLA. While the SOD level increased after GLA administration. Additionally, the attenuation of inflammatory responses by GLA was closely associated with p38MAPK/ERK pathway, and the expressions of protein p-p38MAPK and pERK were inhibited by GLA in LPS-induced ARDS rats.
  
  
  METHODS
  Sixty-four Wistar rats were randomly assigned into control group, Glabridin (GLA) alone group, LPS groups (6 h, 12 h, 24 h), GLA with LPS groups (6 h, 12 h, 24 h). ARDS was induced in rats by intraperitoneal administration of LPS (10 mg/kg). The degree of lung edema was evaluated by calculating the wet/dry weight ratio. The levels of inflammatory mediators, tumor necrosis factor-α (TNF-α) and interleukin-18 (IL-18) were assayed by enzyme-linked immunosorbent assay (ELISA). Surfactant protein A (SPA), malondialdehyde (MDA), nitric oxide (NO) and superoxide dismutase (SOD) were analyzed. Pathological changes of lung tissues were observed by H&E staining. The protein expression of p38MAPK and ERK was detected using immunohistochemical techniques. Lung phosphorylated p38MAPK (p-p38MAPK) and pERK protein expression changes were detected by Western blotting.
  
  
  CONCLUSIONS
  Glabridin significantly ameliorated the lung injury induced by LPS in rats via the inhibition of p38MAPK and ERK signaling pathway, antioxidant effect and reducing inflammation.
authors.affiliation: Department of Critical Care Medicine, The Affiliated Hospital of Innner Mongolia Medical University, Hohhot 010050, China.
authors.forename: Li-Peng
authors.initials: LP
authors.lastname: Zhang
authors.affiliation: Department of Neurology, The People' Hospital of Inner Mongolia, Hohhot 010050 China.
authors.forename: Yan
authors.initials: Y
authors.lastname: Zhao
authors.affiliation: Department of Critical Care Medicine, The Affiliated Hospital of Innner Mongolia Medical University, Hohhot 010050, China.
authors.forename: Guo-Juan
authors.initials: GJ
authors.lastname: Liu
authors.affiliation: Department of Critical Care Medicine, The Affiliated Hospital of Innner Mongolia Medical University, Hohhot 010050, China.
authors.forename: Da-Gang
authors.initials: DG
authors.lastname: Yang
authors.affiliation: Department of Critical Care Medicine, The Affiliated Hospital of Innner Mongolia Medical University, Hohhot 010050, China.
authors.forename: Yi-Huan
authors.initials: YH
authors.lastname: Dong
authors.affiliation: Department of Critical Care Medicine, The Affiliated Hospital of Innner Mongolia Medical University, Hohhot 010050, China.
authors.forename: Li-Hua
authors.initials: LH
authors.lastname: Zhou
mesh_terms: D055371:Acute Lung Injury / Q000139:chemically induced / Q000150:complications / Q000473:pathology; D000818:Animals; D015153:Blotting, Western; D004195:Disease Models, Animal; D004797:Enzyme-Linked Immunosorbent Assay; D007150:Immunohistochemistry; D007529:Isoflavones / Q000494:pharmacology*; D008070:Lipopolysaccharides / Q000633:toxicity; D020935:MAP Kinase Signaling System / Q000187:drug effects*; D008297:Male; D010636:Phenols / Q000494:pharmacology*; D011897:Random Allocation; D051381:Rats; D017208:Rats, Wistar; D012128:Respiratory Distress Syndrome / Q000209:etiology / Q000473:pathology*
chemical_list: D007529:Isoflavones; D008070:Lipopolysaccharides; D010636:Phenols; C107601:glabridin
keywords: ERK; acute respiratory distress syndrome; glabridin; p38MAPK