title: [Role of transient receptor potential canonical 1 in airway remodeling and effect of budesonide on its pulmonary expression in asthmatic guinea pigs].
abstract: OBJECTIVE
  To explore the role of transient receptor potential canonical 1 (TRPC1) in airway remodeling and the effect of budesonide intervention on its expression in the lungs of guinea pigs with ovalbumin-induced asthma.
  
  
  METHODS
  Fifty male guinea pigs were randomized into 5 equal groups, including a blank control group, ovalbumin group, ovalbumin+TRPC1 siRNA group, ovalbumin+luciferase siRNA group, and ovalbumin+budesonide group. After corresponding treatments, bronchoalveolar lavage was collected from the guinea pigs for eosinophils analysis and detection of IL-5 and IL-13 levels using ELISA. The lung tissues were stained with HE and Masson's trichrome to observe the bronchial wall thickness, smooth muscle hypertrophy, subepithelial collagen deposition, and lung inflammations. Immunohistochemistry and real-time quantitative PCR were performed to detect TRPC1 protein and mRNA expressions in the lungs, respectively.
  
  
  RESULTS
  The guinea pig models of ovalbumin-induced asthma showed significantly increased thickness of the bronchial wall, smooth muscle hypertrophy, collagen deposition and inflammatory cell infiltration, but these pathologies were obviously alleviated by treatment with TRPC1 siRNA or budesonide (P/0.05). Immunohistochemstry showed that TRPC1 protein was distributed mainly on the cell membrane and in the nuclei of the basal cells or columnar epithelial cells.
  
  
  CONCLUSIONS
  The up-regulated expression of TRPC1 ion channel is closely associated with the occurrence and progression of airway remodeling and chronic airway inflammation in asthma. Budesonide can partially suppress airway remodeling and inflammation by regulating the expression of TRPC1.
authors.affiliation: Department of Respiratory Medicine, Second Affiliated Hospital of Chongqing Medical University, Chongqing 400010, China. E-mail: linamu90@163.com.
authors.forename: Na
authors.initials: N
authors.lastname: Li
authors.forename: Ye
authors.initials: Y
authors.lastname: He
authors.forename: Min-Chao
authors.initials: MC
authors.lastname: Li
mesh_terms: D056151:Airway Remodeling; D000818:Animals; D001249:Asthma / Q000188:drug therapy / Q000378:metabolism*; D001980:Bronchi / Q000473:pathology; D019819:Budesonide / Q000494:pharmacology*; D004195:Disease Models, Animal; D006168:Guinea Pigs; D007249:Inflammation / Q000378:metabolism; D018793:Interleukin-13 / Q000378:metabolism; D015848:Interleukin-5 / Q000378:metabolism; D007958:Leukocyte Count; D008168:Lung / Q000187:drug effects / Q000378:metabolism; D008297:Male; D010047:Ovalbumin; D050052:TRPC Cation Channels / Q000378:metabolism*
chemical_list: D018793:Interleukin-13; D015848:Interleukin-5; D050052:TRPC Cation Channels; C096351:transient receptor potential cation channel, subfamily C, member 1; D019819:Budesonide; D010047:Ovalbumin