The results demonstrated that NF-κB p65, p-IκBα, TGF-β1, and α-SMA were significantly upregulated and Nrf2 and HO-1 were significantly downregulated in model rats of COPD, indicating the activation of NF-κB, Nrf2, and fibrosis-related signaling pathways. This evidence concerns the gene ACTA1 and chronic obstructive pulmonary disease.