动物造模 z-bio 2021-09-23 796

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

　　Method: 50 male general-grade guinea pigs were randomly divided into 5 groups: group A was a blank control group, group B was an egg protein stimulation group, group C was an egg protein stimulation + TRPC1 siRNA interference group, and group D was an egg protein stimulation + fluorescein Enzyme siRNA intervention group, E group is egg protein stimulation + budesonide interference group. The alveolar lavage fluid (BALF) was collected 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 tissues were collected for hematoxylin-eosin staining (HE) and Marson's trichrome staining (Marson), and image-Pro imaging software was used to quantitatively analyze bronchial wall thickness, smooth muscle proliferation, and collagen deposition. Use immunohistochemical method to observe the relative expression level of TRPC1 protein in the lung. Real-time fluorescent quantitative PCR is used to determine the relative expression of TRPC1 mRNA.

　　Results: Image-Pro imaging software analysis showed that group B had pathologies such as bronchial wall thickening, smooth muscle hyperplasia, basement membrane collagen deposition, inflammatory cell infiltration around the airway, and increased inflammatory factors. Is prominently displayed. The above-mentioned pathological changes in group C and E were not obvious (Pu003c0.05). Further immunohistochemical methods showed that TRPC1 protein is located in the bronchial epithelial mucosa, mainly distributed in the basal cells, cell membranes and columnar epithelial cell nuclei of the bronchial mucosa.

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