动物实验 z-bo 2020-08-22 521

　　Objective: To explore the mechanism of TRPC1 ion channel in the development of airway remodeling, and to interfere with the intervention of budesonide by blocking the expression of transient receptor potential channel C1 (TRPC1).

　　Method: Fifty normal guinea pigs were randomly divided into 5 groups: group A blank control group, group B egg protein stimulation group, group C egg protein stimulation + TRPC1 siRNA interference group, group D: egg protein stimulation + luciferase. siRNA intervention group. E is the egg protein stimulation + budesonide interference group. Alveolar lavage fluid (BALF) was taken 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. The measurement was taken. (ELISA). Bronchopulmonary tissue was stained with hematoxylin-eosin (HE) and Mason, and the bronchial wall thickness, smooth muscle proliferation and collagen deposition were quantitatively analyzed using Image-Pro imaging software. .. Observe the relative expression level of TRPC1 protein in the lung by immunohistochemistry. Real-time fluorescent quantitative PCR was used to determine the relative expression of TRPC1 mRNA.

　　Results: Image-Pro image 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. being shown. Significantly displayed. The above-mentioned pathological changes were not obvious in group C and E (P u003c0.05). In addition, immunohistochemistry showed that TRPC1 protein is located in the bronchial epithelial mucosa, mainly in the basal cells of the bronchial mucosa, the membrane and nucleus of columnar epithelial cells.

　　Conclusion: The high level of TRPC1 channel expression in asthma patients is closely related to the occurrence and development of airway remodeling and chronic airway inflammation. Budesonide regulates the expression of TRPC1 in airway remodeling.