title: The liquid Panax ginseng inhibits epidermal growth factor-induced metalloproteinase 9 and cyclooxygenase 2 expressions via inhibition of inhibitor factor kappa-B-alpha and extracellular signal-regulated kinase in NCI-H292 human airway epithelial cells.
abstract: BACKGROUND
  Ginseng (Panax ginseng C.A. Meyer) has been used in Asian countries for the treatment of various diseases. However, the mechanisms of liquid Panax ginseng (LG) on allergic inflammatory response in epidermal growth factor (EGF)-stimulated human airway epithelial cells remain largely unclear.
  
  
  METHODS
  MUC5AC, cyclooxygenase (COX) 2, and matrix metalloproteinase (MMP) 9 expressions were measured using reverse transcription-polymerase chain reaction, Western blotting, and gelatin zymogram analyses in NCI-H292 cells. Extracellular signal-regulated kinase (ERK) and p38 mitogen-activated protein kinase (MAPK) protein levels were analyzed by Western blotting.
  
  
  RESULTS
  To gain insight into the antiallergy effects of LG, we examined its influence on epidermal growth factor (EGF)-induced MMP-9 and COX-2 productions in NCI-H292 cells. LG was treated for 1 hour and then followed by EGF treatment for 24 hours into NCI-H292 cells. The decrease of COX-2 production was correlated with the reduced levels of proteins and mRNAs of inducible MMP-9 and MUC5AC. LG blocked upstream signaling of NF-kappa-B activation via inhibition of phosphorylations of inhibitor factor-kappa- B-alpha (I-kappa-B-alpha) and ERK. These results suggest that LG protects NCI-H292 cells from EGF-induced damage by down-regulation of COX-2, MMP-9, and MUC5AC gene expressions by blocking NF-kappa-B and ERK.
  
  
  CONCLUSIONS
  LG modulates allergic inflammatory response in EGF-stimulated NCI-H292 human airway epithelial cells via inhibition of I-kappa-B-alpha and ERK.
authors.affiliation: Department of Biocience and Biotechnology, Bio/Molecular Informatics Center, Seoul, Korea.
authors.forename: Jung-Hee
authors.initials: JH
authors.lastname: Kim
authors.forename: Jeong Woo
authors.initials: JW
authors.lastname: Kang
authors.forename: ManSub
authors.initials: M
authors.lastname: Kim
authors.forename: Dong Hun
authors.initials: DH
authors.lastname: Lee
authors.forename: Heejong
authors.initials: H
authors.lastname: Kim
authors.forename: Hee-Sook
authors.initials: HS
authors.lastname: Choi
authors.forename: Eun Jin
authors.initials: EJ
authors.lastname: Kim
authors.forename: Ill-Min
authors.initials: IM
authors.lastname: Chung
authors.forename: Il-Yup
authors.initials: IY
authors.lastname: Chung
authors.forename: Do-Young
authors.initials: DY
authors.lastname: Yoon
mesh_terms: D045744:Cell Line, Tumor; D051546:Cyclooxygenase 2 / Q000235:genetics / Q000378:metabolism*; D004815:Epidermal Growth Factor / Q000276:immunology / Q000378:metabolism; D005786:Gene Expression Regulation / Q000187:drug effects / Q000276:immunology; D006801:Humans; D006967:Hypersensitivity / Q000188:drug therapy*; D051550:I-kappa B Kinase / Q000235:genetics / Q000378:metabolism*; D020780:Matrix Metalloproteinase 9 / Q000235:genetics / Q000378:metabolism*; D048052:Mitogen-Activated Protein Kinase 3 / Q000235:genetics / Q000378:metabolism*; D055271:Mucin 5AC / Q000235:genetics / Q000378:metabolism; D005894:Panax / Q000276:immunology; D010936:Plant Extracts / Q000494:pharmacology; D018517:Plant Roots; D020545:Respiratory Mucosa / Q000187:drug effects* / Q000276:immunology / Q000378:metabolism / Q000473:pathology; D015398:Signal Transduction
chemical_list: C524678:MUC5AC protein, human; D055271:Mucin 5AC; D010936:Plant Extracts; D004815:Epidermal Growth Factor; D051546:Cyclooxygenase 2; D051550:I-kappa B Kinase; D048052:Mitogen-Activated Protein Kinase 3; D020780:Matrix Metalloproteinase 9