Chronic obstructive pulmonary disease (COPD) is a common airway disease, and epithelial mesenchymal transition (EMT) is participated in the pathogenesis of COPD. However, the role of CD147 in COPD remains largely unknown. In order to clarify the role of CD147 in EMT induced by cigarette smoke, we established animal and cell model of EMT by mean of cigarette smoke exposure and detected the expressions of CD147 and EMT markers via PCR, WB and IF. RNA inference was applied to study the role of CD147 in CSE induced EMT in vitro. NAC and H₂O₂ were used to study oxidative stress signaling pathway in this model. As a result, cigarette smoke exposure upregulated the expressions of CD147, α-SMA, and Vimentin and downregulated the expression of Ecadherin and ZO1 both in vivo and in vitro, which was accompanied by augmented level of oxidative stress. CD147 knockdown would partly inhibit CSE induced EMT, while preincubation of H₂O₂ could inverse this effect. In conclusion, CD147 promoted EMT in mice and HBE cells induced by cigarette smoke via oxidative stress signaling pathway.

慢性阻塞性肺疾病（COPD）是一种常见的气道疾病，上皮间质转化（EMT）参与了COPD的发病机制。然而，CD147在COPD中的作用仍然未知。为了阐明CD147在香烟烟雾诱导的EMT中的作用，我们通过香烟烟雾暴露建立了EMT的动物和细胞模型，并通过PCR，WB和IF检测了CD147和EMT标志物的表达。应用RNA干扰技术研究CD147在CSE诱导的EMT中的作用。NAC和H ₂ O ₂用于研究该模型中的氧化应激信号通路。结果，在体内和体外，接触香烟烟雾均上调了CD147，α-SMA和波形蛋白的表达，并下调了Ecadherin和ZO1的表达，并伴有氧化应激水平的升高。CD147敲低将部分抑制CSE诱导的EMT，而H ₂ O _2的预温育可逆转此作用。总之，CD147通过氧化应激信号通路促进香烟烟雾诱导的小鼠和HBE细胞中的EMT 。