title: [Inhibitory effects of apigenin on the expression of GATA-3 and Th2 cytokines in asthmatic mice].
abstract: OBJECTIVE
  To investigate the inhibitory effects and mechanism of apigenin (APG) on dominant response of Th2 cells in asthma model of mice.
  
  
  METHODS
  Thirty-two 6-week-old healthy BALB/c mice, SPF grade, were randomly divided into four groups equally, the normal control group (A), the asthma model group (B), and the two APG groups (C and D) consisted of asthma model mice treated respectively with high-dose (20 mg/kg per day) and low-dose (2 mg/kg per day) APG given by dissolving in 1% dimethyl sulphoxide via intraperitoneal injection. The murine asthma model was established by ovalbumin (OVA) sensitization and provocation. Twenty-four hours after the last airway provocation, acetylcholine (Ach) was administered via caudalis vein for measuring airway resistance by pulmonary function detector; levels of IL- 4 and IL-13 in bronchoalveolar lavage fluid (BALF) and total IgE in serum were determined by enzyme-linked immunosorbent assay (ELISA); total and differential cell counts in BALF were measured by light microscopy; the airway inflammatory infiltration was detected by haematoxylin and eosin (HE) staining; and the signal transducer and activator of transcription 3 (GATA-3) in the lung tissue was determined by Western blot analysis.
  
  
  RESULTS
  As compared with Group A, the airway hyper-reactivity, airway inflammation, cell count and eosinophil percentage in BALF, levels of total serum IgE and BALF IL-4 and IL-13, and GATA-3 protein expression in the lung tissue were significantly increased in Group B (P < 0.05). As compared with Group B, all the above-mentioned indices in Group C and D were lower, showing respective significant difference (P < 0.05), and significant difference was also shown between the two APG treated groups (P < 0.05).
  
  
  CONCLUSIONS
  APG could reduce the airway inflammation and hyper-reactivity by down-regulating the expressions of pulmonary GATA-3 and Th, cytokines, which is a potential drug for asthma therapy.
authors.affiliation: Department of Respiratory Diseases, The First Affiliated Hospital, Nanjing Medical University, Nanjing.
authors.forename: Ling-ling
authors.initials: LL
authors.lastname: Pang
authors.forename: Ruo-ran
authors.initials: RR
authors.lastname: Li
authors.forename: Lin-fu
authors.initials: LF
authors.lastname: Zhou
mesh_terms: D000818:Animals; D047310:Apigenin / Q000494:pharmacology* / Q000627:therapeutic use; D001249:Asthma / Q000188:drug therapy / Q000378:metabolism* / Q000473:pathology; D005260:Female; D050990:GATA3 Transcription Factor / Q000378:metabolism*; D007073:Immunoglobulin E / Q000097:blood; D007249:Inflammation; D018793:Interleukin-13 / Q000378:metabolism*; D015847:Interleukin-4 / Q000378:metabolism*; D051379:Mice; D008807:Mice, Inbred BALB C; D018418:Th2 Cells / Q000378:metabolism
chemical_list: D050990:GATA3 Transcription Factor; C494748:Gata3 protein, mouse; D018793:Interleukin-13; D015847:Interleukin-4; D007073:Immunoglobulin E; D047310:Apigenin