动物造模 z-bio 2021-01-26 318

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

　　Method: 50 ordinary guinea pigs were randomly divided into 5 groups: group A was blank control group, group B was egg protein stimulation group, group C was egg protein stimulation + TRPC1siRNA interference group, group D was egg protein stimulation + luciferase . The siRNA intervention group and the E group are the egg protein stimulation + budesonide intervention group. Collect alveolar lavage fluid (BALF) to compare the proportion 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). The bronchopulmonary tissue was stained with hematoxylin and eosin (HE) and Merson (Merson). Image-Pro image processing software is used to quantitatively analyze bronchial wall thickness, smooth muscle proliferation and collagen deposition. The relative expression level of TRPC1 protein in the lung was observed by immunohistochemistry. Real-time fluorescent quantitative PCR was used to determine the relative expression of TRPC1 mRNA.

　　Result: Image-Pro imaging software analysis showed that group B had pathological changes, such as bronchial wall thickening, smooth muscle hyperplasia, basement membrane collagen deposition, inflammatory cell infiltration around the airway, and increased inflammatory factors, which is meaningful. . The above pathological changes in group C and E were not obvious (P\u003c0.05). Further immunohistochemistry showed that TRPC1 protein is located in the bronchial epithelial mucosa, mainly distributed in the basal cells of the bronchial mucosa, columnar epithelial cell membrane and cell nucleus.

　　Conclusion: The high level of TRPC1 channel expression in asthma patients is closely related to airway remodeling and the development of chronic airway inflammation. Budesonide can participate in airway remodeling to a certain extent by regulating the expression of TRPC1 evolution.