动物造模 z-bio 2022-07-21 344

　　Objective: To explore the mechanism of TRPC1 ion channel in the evolution of airway remodeling and the intervention effect of budesonide by interfering with the expression of transient receptor potential channel C1 (TRPC1).

　　Methods: Fifty male ordinary guinea pigs were randomly divided into 5 groups: group A was blank control group, group B was ovalbumin stimulation group, group C was ovalbumin stimulation + TRPC1 siRNA interference group, and group D was ovalbumin stimulation + Luciferase siRNA intervention group and E group were ovalbumin stimulation + budesonide interference group. The bronchoalveolar lavage fluid (BALF) was collected to compare the percentage of eosinophils (Eos) in the total number of cells; the expression levels of IL-5 and IL-13 in BALF were determined by enzyme-linked immunosorbent assay (ELISA). Bronchopulmonary tissues were collected for hematoxylin-eosin staining (HE) and Masson's trichrome staining (Maason), and Image-Pro image processing software was used to quantitatively analyze bronchial wall thickness, smooth muscle proliferation and collagen deposition. The relative expression level of TRPC1 protein in lung was observed by immunohistochemistry. The relative expression of TRPC1 mRNA was determined by real-time quantitative PCR.

　　RESULTS: Image-Pro image software analysis results showed that group B significantly showed pathological changes such as bronchial wall thickening, smooth muscle proliferation, basement membrane collagen deposition, inflammatory cell infiltration around the airway, and increased inflammatory factors. Pathological changes were not obvious (P<0.05). Further immunohistochemistry showed that TRPC1 protein was located in the bronchial epithelial mucosa, mainly distributed in the basal cells of the bronchial mucosa, and in the membrane and nucleus of the columnar epithelial cells.

　　Conclusion: The high-level expression of TRPC1 channel in asthmatic individuals is closely related to the occurrence and development of airway remodeling and chronic airway inflammation; budesonide can participate in the evolution of airway remodeling by regulating the expression of TRPC1 to a certain extent.