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. Conclusion 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.