Objective: To explore the significance of CC16 in the pathogenesis of chronic obstructive pulmonary disease(COPD)by examining the CC16 expression in the airway epithelium of COPD rats before and after Tiotropium intervention. Methods: The male Sprague-Dawley(SD)rats were randomly assigned into the healthy control group, COPD model group(smoke+endotoxin), and Tiotropium intervention group, with 10 in each. RT-PCR was used to detect the gene expression of CC16 mRNA and immunohistochemistery was applied to test the protein expression of CC16 in the lung tissue in each group of rats. Enzyme-linked immunosorbent assay(ELISA)was adopted to investigate the levels of CC16, PLA2, IL8 and TNFα in the serum as well as PLA2, IL8, and TNFα in the lung tissue. Results: CC16 mRNA gene expression was significantly reduced in the lung tissue of COPD model group compared with the healthy control group, but remarkably increased in Tiotropium intervention group as opposed to COPD model group. CC16 was found to be higher in the serum and lung tissue of COPD model group and PLA2, IL8 and TNFα were lower than those in the healthy control group, while CC16 level was shown to be markedly elevated in the serum and lung tissue of Tiotropium intervention group and PLA2, IL8, and TNFα levels were significantly lower when compared with COPD model group. The differences were statistically significant(P<0.05). Conclusion: Gene expression of CC16 mRNA and CC16 protein expression in the airway epithelium decreased in the development of COPD rats, which may be a histological marker of mild airway injury in pathogenesis of COPD and involved in the development and progression of COPD. |
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