摘要：Background Chronic obstructive pulmonary disease(COPD)is a severe public health *** smoke(CS)is a risk factor for COPD and lung *** underlying molecular mechanisms of CS-induced malignant transformation of bronchial epithelial cells remain *** this study,we describe a lung-on-a-chip to explore the possible mechanistic link between cigarette smoke extract(CSE)-associated COPD and lung *** An in vitro lung-on-a-chip model was used to simulate pulmonary epithelial cells and vascular endothelial cells with *** levels of IL-6 and TNF-αwere tested as indicators of inflammation using an enzyme-linked immune sorbent *** junction complex mRNA expression was detected with qRT-PCR as the index of epithelial-to-mesenchymal transition(EMT).The effects of CSE on the phosphorylation of signal transduction and transcriptional activator 3(STAT3)were detected by Western *** cytometry was performed to investigate the effects of this proto-oncogene on cell cycle *** Inflammation caused by CSE was achieved in a lung-on-a-chip model with a mimetic *** exposure induced the degradation of intercellular connections and triggered the EMT *** exposure also activated the phosphorylation of proto-oncogene STAT3,while these effects were inhibited with *** CSE exposure in the lung-on-a-chip model caused activation of STAT3 in epithelial cells and endothelial ***0152,an inhibitor of activated STAT3,could be a potential treatment for CS-associated COPD and lung cancer.