title: [The effect of cyclosporine A on lipopolysaccharide-induced acute lung injury in mice].
abstract: OBJECTIVE
  To investigate the effect of mitochondrial permeability transition pore inhibitor cyclosporine A (CsA) on lipopolysaccharide (LPS)-induced acute lung injury in mice.
  
  
  METHODS
  All male ICR mice were randomly divided into five groups (n = 24): control group, LPS group, dexamethasone group, cyclosporine A(CsA) group and CsA + atractyloside(Atr) group. Six hours after treatment with LPS, the activity of lactate dehydrogenlase (LDH) in bronchoalveolar lavage fluid (BALF) and level of tumor necrosis factor-alpha (TNF-alpha) in lung tissue were detected. The lung wet weight/dry weight ratio and the pulmonary capillary permeability index were also detected.
  
  
  RESULTS
  In contrast to LPS group, the mitochondrial permeability transition pore inhibitor CsA induced a decrease in LDH activity in the BALF and TNF-alpha level in lung tissue, lung wet weight/dry weight ratio and the pulmonary capillary permeability index were declined. Atractyloside, the activator of mitochondrial permeability transition pore, almost abolished the role of CsA on LPS-induced lung injury.
  
  
  CONCLUSIONS
  These results suggested that CsA plays the protective effect on LPS-induced lung injury in mice, it is likely through inhibiting the opening of mitochondrial permeability transition pore.
authors.affiliation: Department of Respiratory Medicine, The first affiliated Hospital of Bengbu Medical College, Bengbu 233004, China.
authors.forename: Jun-Feng
authors.initials: JF
authors.lastname: Hu
authors.forename: Xue-Mei
authors.initials: XM
authors.lastname: Xia
authors.forename: Dian-Ming
authors.initials: DM
authors.lastname: Li
authors.forename: Yong
authors.initials: Y
authors.lastname: Zhang
authors.forename: Yu-Qing
authors.initials: YQ
authors.lastname: Chen
mesh_terms: D055371:Acute Lung Injury / Q000139:chemically induced / Q000503:physiopathology / Q000517:prevention & control*; D000818:Animals; D016572:Cyclosporine / Q000494:pharmacology*; D007770:L-Lactate Dehydrogenase / Q000378:metabolism; D008070:Lipopolysaccharides; D008297:Male; D051379:Mice; D008813:Mice, Inbred ICR; D033681:Mitochondrial Membrane Transport Proteins / Q000037:antagonists & inhibitors; D000083162:Mitochondrial Permeability Transition Pore; D020011:Protective Agents / Q000494:pharmacology*; D014409:Tumor Necrosis Factor-alpha / Q000378:metabolism
chemical_list: D008070:Lipopolysaccharides; D033681:Mitochondrial Membrane Transport Proteins; D000083162:Mitochondrial Permeability Transition Pore; D020011:Protective Agents; D014409:Tumor Necrosis Factor-alpha; D016572:Cyclosporine; D007770:L-Lactate Dehydrogenase