动物造模,慢性阻塞性肺疾病 z-bio 2021-09-17 325

　　Objective: To study the effect of recombinant rat CC16 (rCC16) protein on reducing lung tissue damage in a mouse model of chronic obstructive pulmonary disease, and on matrix metalloproteinase (MMP)-9 and tissue inhibitor of matrix metalloproteinase (TIMP) in lung tissue -1 Regulation of expression.

　　Methods: Forty clean C57BL/6 mice were randomly divided into 4 groups, namely blank group, COPD model group, rCC16 dose group 1 and dose group 2. Except for the blank group, all the other mice were smoked for 3 months. The COPD model was prepared. From the third month, the blank group and the model group were given PBS nasal drops, and the rCC16 dose group 1 and dose group 2 were given 1μg/g body weight and 2.5μg/g body weight respectively. Mental state, diet, weight change, urine and feces, etc., H&E staining to observe the morphological and structural changes of the lung tissue of each group of mice, fluorescence quantitative polymerase chain reaction, immunohistochemistry to detect MMP-9 and TIMP-1 messenger RMA ( mRNA) and protein expression changes.

　　Results: The weight of the mice in the blank group increased with the feeding cycle. The weight of the mice in the COPD group was significantly reduced compared with the blank group. After the rCC16 intervention group, the weight of the intervention group 2 mice increased week by week, but the intervention group 1 mouse weight increased slowly The difference was statistically significant (P<0.05); the lung tissue structure of the COPD model group was significantly damaged, the alveolar interval was widened, and emphysema was partially formed. After the rCC16 intervention group, the alveolar structure of the lungs of the mice tended to be intact , The formation of pulmonary bullae was also reduced; the expressions of MMP-9 and TIMP-1 in the lung tissues of the COPD model group were significantly higher than those of the blank group (P<0.05); after the intervention of rCC16, both MMP-9 and TIMP- The expression of 1, the difference was statistically significant (P<0.05). The reduction effect of rCC16 on MMP-9 was dose-dependent, while the regulation of TIMP-1 was not dose-dependent.

　　Conclusion: RCC16 nasal drip intervention can reduce lung tissue damage in COPD mice and reduce the expression of MMP-9 and TIMP-1 in lung tissue, which has positive significance for the treatment of COPD.