动物造模,慢阻肺大鼠气道炎症 z-bio 2022-12-13 280

　　Objective To investigate the effects of metformin (Met) on airway inflammation in rats with chronic obstructive pulmonary disease (COPD).

　　Methods The COPD rat model was established by smoking for 30 min every day for 30 days, and 2 mL lipopolysaccharide (LPS) solution was instilled into the airway on the 1st, 14th and 28th days. The effect of Met on the level of miR-34a in lung tissue was detected by real-time quantitative PCR (qRT-PCR); The number of leukocytes in bronchoalveolar lavage fluid (BALF) and wright staining were used to detect the influence of Met on it; Hematoxylin eosin (HE) was used to detect the influence of Met on lung tissue morphology; Enzyme linked immunosorbent assay (ELISA) for detection of interleukin-6, interleukin-8 and interleukin-1 in serum by Met β、 Tumor necrosis factor- α (TNF- α) The impact of the level; The effect of Met on sirt1 protein level in lung tissue was detected by Western blot; TargetScan searched the 3 ′ UTR and miR-34a binding sites of sirt1 mRNA, and identified them by the double luciferase reporter gene detection kit.

　　Results Compared with the control group, the level of sirt1 protein in lung tissue, the ratio of monocytes to macrophages, the level of miR-34a, the number of white blood cells in BALF, the ratio of neutrophils, eosinophils and lymphocytes, and the levels of IL-6, IL-8, IL-1 in serum in the model group decreased (P<0.05) β、 TNF- α The level increased (P<0.05); Met can alleviate the sirt1 protein level in lung tissue, decrease the monocyte macrophage ratio, miR-34a level, the number of white blood cells in BALF, the proportion of neutrophils, eosinophils and lymphocytes, and IL-6, IL-8, IL-1 in serum β、 TNF- α The level increased (P<0.05); Increasing the level of miR-34a reverses the effect of Met on COPD rats. There was a targeting relationship between miR-34a and sirt1 by double luciferase.

　　Conclusion Met can down regulate miR-34a and up regulate sirt1 to alleviate the airway inflammation of COPD, which provides some experimental basis and evidence for clinical treatment of COPD with Met.