IL-17/NF-κB p65 promotes the bronchial epithelial-mesenchymal transition of COPD mice
Objective To explore the role of interleukin 17(IL-17)/nuclear factor-κB p65(NF-κB p65)pathway in bronchial epithelial-mesenchymal transition(EMT)of chronic obstructive pulmonary disease(COPD).Methods 8 mice were respectively in the control group and COPD group.COPD mice model was induced by cigarette smoking.The lung tissues from mice were paraffin embedded and sliced.The slides were stained with HE to observe the pathologic change in bronchi and pulmonary,and then analyzed the destructive index and mean linear intercept(MLI).The expressions of E-cadherin and Vimentin were assessed using double immunofluorescence staining.The expressions of IL-17 and NF-κB p65 were measured by immunohistochemistry.Results The destructive index and MLI in the COPD group were significantly larger than that in control group,showing a statistically significant difference(P<0.05),and indicating that the pathological histology is consistent with the changes in COPD.Compared with the control group,in bronchi and pulmonary from COPD group,the expression of E-cadherin was significantly decreased(P<0.05),indicating an enhanced epithelial mesenchymal transition in the bronchopulmonary tissue of COPD group mice.The expressions of IL-17 and NF-κB p65 were significantly higher in COPD group than the control group(P<0.05).Moreover,the expression of IL-17 and NF-κB p65 were negatively correlated with the E-cadherin expression,but positively correlated with the Vimentin expression.Conclusion IL-17/NF-κB p65 pathway may promote bronchial EMT of COPD mice.That finding could contribute to understanding the pathogenesis of airway remodeling in COPD,provide novel strategy in treatment for COPD inflammation and prevent COPD patients from lung cancer.
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