【Animal Modeling】-Effect of Qingzao Jiufei Decoction and its decomposers on pulmonary inflammation-related factors in mice infected with Mycoplasma pneumoniae

  Objective: To investigate the effect of Qingzao Jiufei Decoction (QJD) and its decomposers on the content of TNF-α?INF-γ in serum and the expression of MPN372?P1?AQP5 in lung tissue of mice infected with Mycoplasma pneumoniae (MP), and to clarify its anti-inflammatory effect. Molecular mechanism of MP infection?

  Methods: 144 SPF grade BABL/c mice were randomly divided into normal group (group A), model group (group B), QJD group (group C), QJD decomposer group I (group D), and QJD decomposer II group (E group) and azithromycin group (F group), 24 mice in each group? Except group A, the other 5 groups of mice were treated with MP infection model. On the 3rd, 7th, 10th, and 14th days, the samples were collected. The pathological sections of the mouse lung tissue were observed under the microscope, and the pathological inflammation degree of the mouse lung tissue was scored; the lung index and the dry-wet ratio of the mice were calculated; the MPN372? P1 gene content was measured; enzyme-linked immunosorbent assay (ELISA) was used to measure the changes of serum TNF-α and INF-γ levels of mice in each group; Western blot was used to detect the expression of AQP5 protein.

  Results: After MP infection, the alveolar septum was thickened, the bronchiolar wall was thickened, and a large number of inflammatory cells were infiltrated; the lung index was increased, and the dry-wet ratio was decreased; the content of TNF-α and INF-γ showed an increasing trend. and peaked on the 7th day; the protein expression of AQP5 showed a downward trend and gradually increased from the 14th day; compared with the B group, from the 7th day, the C group could down-regulate the expression levels of MPN372?P1 and TNF-α. , up-regulated the expression level of INF-γ?AQP5; the effect of group D was mainly manifested in down-regulating the expression of MPN372?P1?TNF-α, and the effect of group E was mainly manifested in up-regulating the expression of INF-γ?AQP5?

  Conclusion: QJD can control the pulmonary inflammation after MP infection, reduce the production of MP toxin MPN372 and the expression of P1 adhesion protein; up-regulate the expression of INF-γ and AQP5 protein and down-regulate the expression of TNF-α, which is one of its mechanisms?