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10.1038/srep11758

http://scihub22266oqcxt.onion/10.1038/srep11758
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suck abstract from ncbi


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pmid26156213
      Sci+Rep 2015 ; 5 (ä): 11758
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  • Galangin attenuates airway remodelling by inhibiting TGF-?1-mediated ROS generation and MAPK/Akt phosphorylation in asthma #MMPMID26156213
  • Liu YN ; Zha WJ ; Ma Y ; Chen FF ; Zhu W ; Ge A ; Zeng XN ; Huang M
  • Sci Rep 2015[Jul]; 5 (ä): 11758 PMID26156213 show ga
  • Galangin, a natural flavonol, has attracted much attention for its potential anti-inflammatory properties. However, its role in the regulation of airway remodelling in asthma has not been explored. The present study aimed to elucidate the effects of galangin on chronic inflammation and airway remodelling and to investigate the underlying mechanisms both in vivo and in vitro. Ovalbumin (OVA)-sensitised mice were administered with galangin 30?min before challenge. Our results showed that severe inflammatory responses and airway remodelling occurred in OVA-induced mice. Treatment with galangin markedly attenuated the leakage of inflammatory cells into bronchoalveolar lavage fluid (BALF) and decreased the level of OVA-specific IgE in serum. Galangin significantly inhibited goblet cell hyperplasia, collagen deposition and ?-SMA expression. Lowered level of TGF-?1 and suppressed expression of VEGF and MMP-9 were observed in BALF or lung tissue, implying that galangin has an optimal anti-remodelling effect in vivo. Consistently, the TGF-?1-induced proliferation of airway smooth muscle cells was reduced by galangin in vitro, which might be due to the alleviation of ROS levels and inhibition of MAPK pathway. Taken together, the present findings highlight a novel role for galangin as a promising anti-remodelling agent in asthma, which likely involves the TGF-?1-ROS-MAPK pathway.
  • |Actins/metabolism [MESH]
  • |Airway Remodeling/*drug effects [MESH]
  • |Animals [MESH]
  • |Asthma/immunology/*metabolism/*pathology [MESH]
  • |Bronchoalveolar Lavage Fluid/cytology/immunology [MESH]
  • |Cell Proliferation/drug effects [MESH]
  • |Collagen/metabolism [MESH]
  • |Disease Models, Animal [MESH]
  • |Female [MESH]
  • |Fibrosis [MESH]
  • |Flavonoids/*pharmacology [MESH]
  • |Goblet Cells/metabolism/pathology [MESH]
  • |Humans [MESH]
  • |Hyperplasia [MESH]
  • |Immunoglobulin E/blood/immunology [MESH]
  • |Matrix Metalloproteinase 9/metabolism [MESH]
  • |Mice [MESH]
  • |Mitogen-Activated Protein Kinases/*metabolism [MESH]
  • |Myocytes, Smooth Muscle/drug effects/metabolism [MESH]
  • |Ovalbumin/adverse effects [MESH]
  • |Oxidation-Reduction/drug effects [MESH]
  • |Phosphorylation [MESH]
  • |Proto-Oncogene Proteins c-akt/*metabolism [MESH]
  • |Reactive Oxygen Species/*metabolism [MESH]
  • |Signal Transduction/drug effects [MESH]
  • |Transforming Growth Factor beta1/*metabolism [MESH]


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