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10.12659/msm.900452

http://scihub22266oqcxt.onion/10.12659/msm.900452
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C5445901!5445901 !28522797
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suck abstract from ncbi


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pmid28522797
      Med+Sci+Monit 2017 ; 23 (ä): 2357-2364
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  • Protective Effects of Hydrogen-Rich Saline Against Lipopolysaccharide-Induced Alveolar Epithelial-to-Mesenchymal Transition and Pulmonary Fibrosis #MMPMID28522797
  • Dong WW ; Zhang YQ ; Zhu XY ; Mao YF ; Sun XJ ; Liu YJ ; Jiang L
  • Med Sci Monit 2017[May]; 23 (ä): 2357-2364 PMID28522797 show ga
  • BACKGROUND Fibrotic change is one of the important reasons for the poor prognosis of patients with acute respiratory distress syndrome (ARDS). The present study investigated the effects of hydrogen-rich saline, a selective hydroxyl radical scavenger, on lipopolysaccharide (LPS)-induced pulmonary fibrosis. MATERIAL AND METHODS Male ICR mice were divided randomly into 5 groups: Control, LPS-treated plus vehicle treatment, and LPS-treated plus hydrogen-rich saline (2.5, 5, or 10 ml/kg) treatment. Twenty-eight days later, fibrosis was assessed by determination of collagen deposition, hydroxyproline, and type I collagen levels. Development of epithelial-to-mesenchymal transition (EMT) was identified by examining protein expressions of E-cadherin and ?-smooth muscle actin (?-SMA). Transforming growth factor (TGF)-?1 content, total antioxidant capacity (T-AOC), malondialdehyde (MDA) content, catalase (CAT), and superoxide dismutase (SOD) activity were determined. RESULTS Mice exhibited increases in collagen deposition, hydroxyproline, type I collagen contents, and TGF-?1 production in lung tissues after LPS treatment. LPS-induced lung fibrosis was associated with increased expression of ?-SMA, as well as decreased expression of E-cadherin. In addition, LPS treatment increased MDA levels but decreased T-AOC, CAT, and SOD activities in lung tissues, indicating that LPS induced pulmonary oxidative stress. Hydrogen-rich saline treatment at doses of 2.5, 5, or 10 ml/kg significantly attenuated LPS-induced pulmonary fibrosis. LPS-induced loss of E-cadherin in lung tissues was largely reversed, whereas the acquisition of ?-SMA was dramatically decreased by hydrogen-rich saline treatment. In addition, hydrogen-rich saline treatment significantly attenuated LPS-induced oxidative stress. CONCLUSIONS Hydrogen-rich saline may protect against LPS-induced EMT and pulmonary fibrosis through suppressing oxidative stress.
  • |Animals [MESH]
  • |Cadherins/metabolism [MESH]
  • |Collagen Type I/metabolism [MESH]
  • |Collagen/metabolism [MESH]
  • |Epithelial Cells/metabolism [MESH]
  • |Epithelial-Mesenchymal Transition/drug effects [MESH]
  • |Fibrosis [MESH]
  • |Hydrogen/*therapeutic use [MESH]
  • |Hydroxyproline/metabolism [MESH]
  • |Lipopolysaccharides [MESH]
  • |Lung/pathology [MESH]
  • |Male [MESH]
  • |Mice [MESH]
  • |Mice, Inbred ICR [MESH]
  • |Oxidative Stress/drug effects [MESH]
  • |Pulmonary Fibrosis/prevention & control/*therapy [MESH]
  • |Respiratory Distress Syndrome/therapy [MESH]
  • |Sodium Chloride/*therapeutic use [MESH]


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