Effects of recombinant CC16 protein on lung tissue structure and expression of MMP-9 and TIMP-1 in mice with chronic obstructive pulmonary disease

  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 (COPD), and on matrix metalloproteinase (MMP)-9 and matrix in lung tissue Regulating the expression of tissue inhibitor of metalloproteinases (TIMP)-1.

  Method: 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. The rCC16 dose group 1 and dose group 2 were given 1μg/g body weight and 2.5μg/g body weight respectively for the intervention of rCC16 nose drops. Observe each group of mice Mental status, diet, weight changes, urine and feces, etc., H&E staining to observe the changes in lung tissue morphology and structure of each group of mice, fluorescent 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 less than that in the blank group. After the rCC16 intervention group, the weight of the mice in the intervention group 2 increased week by week, but the mice in the intervention group 1 increased slowly , The difference was statistically significant (P<0.05); the lung tissue structure of the mice in the COPD model group was significantly destroyed, the alveolar interval widened, and some emphysema 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 tissue of the COPD model group were significantly higher than those in 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 is of positive significance for the treatment of COPD.