title: [Effect of triptolide on airway remodeling and the expression of phosphoinositide 3-kinases in asthmatic rats].
abstract: OBJECTIVE
  To explore the effect of Triptolide on airway remodeling and the expression of Phosphoinositide 3-Kinases in asthmatic rats.
  
  
  METHODS
  40 rats were randomly divided into 5 groups (n = 8): (1) Control group; (2) Asthmatic 4 weeks group; (3) Asthmatic 6 weeks group; (4) Therapeutic 4 weeks group; (5) Therapeutic 6 weeks group. The airway resistance and eosinophilic inflammation of airway wall were observed. The airway wall thickness (WA/Pi), the bronchial smooth muscle thickness (smooth muscle area/Pi) and the number of bronchial smooth muscle nucleus (N/Pi) were measured by image analysis system. The expression of PI3K protein and mRNA were determined by immunohistochemical staining and reverse transcription-polymerase chain reaction (RT-PCR).
  
  
  RESULTS
  (1) The expression of PI3K p85alpha protein and mRNA in asthmatic 4 weeks group and asthmatic 6 weeks group were significantly higher than control group, respectively (P < 0.01). The above-mentioned parameters of therapeutic 6 weeks group were significantly lower than those of asthmatic 4 weeks group, asthmatic 6 weeks group and therapeutic 4 weeks group, respectively (P < 0.01, P < 0.01 P < 0.05). (2) The WA/Pi, the smooth muscle area/Pi and the N/Pi of asthmatic 4 weeks group and asthmatic 6 weeks group were significantly higher than control group, respectively (P < 0.01). The above-mentioned parameters of therapeutic 6 weeks group were significantly lower than those of asthmatic 4 weeks group, asthmatic 6 weeks group and therapeutic 4 weeks group, respectively (P < 0.01). (3) The airway resistance of asthmatic 4 weeks group and asthmatic 6 weeks group were significantly higher than the control group, respectively (P < 0.01). The above-mentioned parameters of therapeutic 6 weeks group were significantly lower than those of asthmatic 4 weeks group, asthmatic 6 weeks group and therapeutic 4 weeks group, respectively (P < 0.01, P < 0.01, P < 0.05).
  
  
  CONCLUSIONS
  The proliferation of airway smooth muscle is a remarkable character of airway remodeling in asthma. The PI3K signal pathway may be involved in the process. Triptolide may reduce AHR and decrease the proliferation of ASMCs by inhibiting the expression of PI3K. It may have potential therapeutic effects in the asthmatic airway remodeling.
authors.affiliation: Department of Respiratory Medicine, Hospital Affiliated Guilin Medical College, Guilin 541001, China.
authors.forename: Bi-Wen
authors.initials: BW
authors.lastname: Mo
authors.forename: Chang-Ming
authors.initials: CM
authors.lastname: Wang
authors.forename: Zhen-Xiang
authors.initials: ZX
authors.lastname: Zhang
authors.forename: Yong-Jian
authors.initials: YJ
authors.lastname: Xu
authors.forename: Wei-Ning
authors.initials: WN
authors.lastname: Xiong
authors.forename: Xian-Sheng
authors.initials: XS
authors.lastname: Liu
authors.forename: Chun-Sheng
authors.initials: CS
authors.lastname: Fang
mesh_terms: D056151:Airway Remodeling; D000818:Animals; D001249:Asthma / Q000378:metabolism* / Q000503:physiopathology*; D004224:Diterpenes / Q000494:pharmacology*; D004852:Epoxy Compounds / Q000494:pharmacology; D008297:Male; D010616:Phenanthrenes / Q000494:pharmacology*; D058539:Phosphatidylinositol 3-Kinase / Q000378:metabolism*; D051381:Rats; D017207:Rats, Sprague-Dawley; D015398:Signal Transduction
chemical_list: D004224:Diterpenes; D004852:Epoxy Compounds; D010616:Phenanthrenes; C001899:triptolide; D058539:Phosphatidylinositol 3-Kinase