title: Research on the molecular mechanism of Seretide treatment to asthma disease.
abstract: BACKGROUND
  Asthma is one of the most common chronic diseases in children. It is attributable to complicated coactions between various genetic factors and environmental allergens.
  
  
  OBJECTIVE
  We attempt to unfold the mechanism of asthmatic disorder and research the molecular mechanism of Seretide on asthmatic disease.
  
  
  METHODS
  Using the GSE31773 microarray datasets downloaded from Gene Expression Omnibus database, we first screened the differentially expressed genes between healthy control and asthmatic samples cells based on classical t-test and false discovery rate < 0.05 as significant threshold. The underlying molecular mechanisms were investigated by Kyoto Encyclopedia of Genes and Genomes pathway enrichment analysis. In addition, the crosstalk network of pathways was also constructed.
  
  
  RESULTS
  A total of 2011 differentially expressed genes were obtained by comparing asthmatic sample treated with Seretide and healthy controls. A total of 403 differentially expressed genes were collected between asthma samples untreated by Seretide and healthy sample controls. The enriched pathway of differentially expressed genes included signal transduction disorder (such as TGF-beta signaling pathway) and metabolism disorder (such as Phenylalanine metabolism). There were 27 pathway crosstalk pairs among 13 pathways.
  
  
  CONCLUSIONS
  Our findings will help to clarify the molecular mechanism of Seretide and offer advices for asthma pathogenesis, Seretide therapy and follow-up treatment.
authors.affiliation: Department of Respiratory Medicine, Shanghai Jiao Tong University, Shanghai, China.
authors.forename: Z-W
authors.initials: ZW
authors.lastname: Liu
authors.forename: F
authors.initials: F
authors.lastname: Yue
authors.forename: F-Y
authors.initials: FY
authors.lastname: Gao
authors.forename: Y-B
authors.initials: YB
authors.lastname: Qian
authors.forename: R-L
authors.initials: RL
authors.lastname: Wang
mesh_terms: D000420:Albuterol / Q000031:analogs & derivatives* / Q000494:pharmacology / Q000627:therapeutic use; D000730:Androstadienes / Q000494:pharmacology* / Q000627:therapeutic use; D018927:Anti-Asthmatic Agents / Q000494:pharmacology* / Q000627:therapeutic use; D001249:Asthma / Q000188:drug therapy / Q000235:genetics*; D016022:Case-Control Studies; D030541:Databases, Genetic / Q000706:statistics & numerical data*; D004338:Drug Combinations; D000068297:Fluticasone-Salmeterol Drug Combination; D015870:Gene Expression / Q000187:drug effects*; D020869:Gene Expression Profiling / Q000379:methods / Q000706:statistics & numerical data; D006801:Humans; D008957:Models, Genetic; D058990:Molecular Targeted Therapy / Q000379:methods* / Q000706:statistics & numerical data; D015398:Signal Transduction / Q000187:drug effects / Q000235:genetics*
chemical_list: D000730:Androstadienes; D018927:Anti-Asthmatic Agents; D004338:Drug Combinations; D000068297:Fluticasone-Salmeterol Drug Combination; D000420:Albuterol