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YANG Jinghuan^a , LI linqiao^a, QIN Qihua^ab , CHU Shuyuan^b

( a. Department of Respiratory and Critical Care Medicine , b, Laboratory of Respiratory Disease .Affiliated Hospital of Guilin Medical University, Guilin 

541001, China)

Abstract Objective To explore the role of interleukin 17(IL-17)/nuclear factor-¦ÊB p65( NF-¦ÊB p65 ) pathway in bronchial epithelial-mesenchymal transition(EMT)of chronic obstructive pulmonary disease( COPD ).IMethods 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 toobserve the pathologic change in bronchi and pulmonary, and then analyzed the destructive index and mean linealintercept ( MLI). The expressions of E-cadherin and Vimentin were assessed using double immunofluorescencestaining. The expressions of IL-17 and NF-¦ÊB p65 were measured by immunohistochemistry. Results The destructiveindex and MLI in the COPD group were significantly larger than that in control group, showing a statisticallysignificant 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-cadherinwas significantly decreased ( P< 0. 05 ), indicating an enhanced epithelial mesenchymal transition in thebronchopulmonary tissue of COPD group mice. The expressions of IL-17 and NF-¦ÊB p65 were significantly higher inCOPD group than the control group ( P<0.05 ). Moreover, the expression of IL-17 and NF-¦ÊB p65 were negativelcorrelated with the E-cadherin expression, but positively correlated with the Vimentin expression. Conclusion IL-17/NF-¦ÊB p65 pathway may promote bronchial EMT of COPD mice. That finding could contribute to understanding thepathogenesis of airway remodeling in COPD, provide novel strategy in treatment for COPD inflammation and prevent COPD patients from lung cancer.

Keywords.chronic obstructive pulmonary disease; interleukin 17; nuclear factor-¦ÊB p65; epithelial-mesenchymaltransition

DOI:10.19296/i.cnki.1008-2409.2024-04-006

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