动物造模,药效评价,支气管哮喘 z-bio 2024-08-22 436

　　(1) The replication method mainly utilizes transgenic or gene knockout techniques to study the role of changes in certain gene expression products in the development of asthma.

　　(2) Model features

　　1) The transcription factor GATA-3 transgenic mice model showed reduced synthesis of IL-4, IL-5, and interleukin-13 (IL-13), as well as significantly reduced airway EOS infiltration, mucus secretion, and IgE synthesis induced by sensitization. GATA-3 regulates the expression of Th2 cytokines, and eliminating GATA-3 activity can slow down Th2 cell responses, making it a potential new target for asthma treatment.

　　2) CD23 transgenic and gene knockout mice with anti-CD23 antibodies can inhibit IgE and IgG1 synthesis in OVA induced Balc/c mouse asthma models, prevent pulmonary EOS infiltration and AHR production. However, the degree of EOS infiltration and increased airway hyperresponsiveness induced by sensitization in CD23 transgenic mice was significantly negatively correlated with CD23 expression in T and B cells. The asthma manifestations induced by CD23-/- (gene knockout) mice are also more severe than those induced by CD23+/+mice, indicating that CD23 not only promotes asthma, but may also have a negative regulatory effect on allergic reactions and AHR.

　　(3) Comparative medicine bronchial asthma is a chronic airway inflammation involving various inflammatory cells such as eosinophils (EOS), mast cells, and T lymphocytes, which leads to airway hyperresponsiveness (AHR) in patients, resulting in airway obstruction and airflow limitation. The pathogenesis of bronchial asthma is complex. Given the limitations of direct human trials, animal experiments are required to determine the etiology, explore the pathogenesis, evaluate new treatment methods, and develop new drugs to a considerable extent. Therefore, the establishment of a bronchial asthma animal model provides a tool for further research.