〔Abstract〕 Objective To investigate the molecular mechanisms of inflammatory response and mucus hypersecretion of N-Acetyl-L-cysteine(NAC)or Resolvin-D1(RvD1)inhibiting hydrogen peroxide(H2O2)-induced diseased human bronchial epithelial cell of chronic obstructive pulmonary disease(COPD)primary airway epithelial cells(DHBE)of inflammation and mucus hypersecretion. Methods DHBE cells were isolated, identified and cultured. The oxidative stress model was established with the optimum stimulation concentration of H2O2by stimulating DHBE and incubated with NAC and RvD1in vitro. Reactive oxygen species(ROS) were measured by immunofluorescence and flow cytometry; IKKβ and NF-κB protein expressions and the phosphorylation level were detected respectively by Western blot; the mRNA expression and secretion levels of tumor necrosis factor(TNF)-α and interleukin(IL)-8 were detected by ELISA and qRT-PCR; mucin 5 AC(MUC5 AC) protein expression was detected by qRT-PCR and immunofluorescence. Results Compared with the control group, H2O2stimulated DHBE could significantly increase the production of ROS(P<0.05), the expressions of IKKβ and NF-κB phosphorylation increased in a concentration-dependent manner(P<0.05), The intracellular mRNA levels of TNF-α, IL-8 and protein levels of TNF-α, IL-8 in cell culture medium increased(P<0.05), MUC5 AC expression increased(P<0.05). NAC and RvD1 could significantly inhibit the expression of TNF-α, IL-8 and MUCSAC induced by H2O2(P<0.05). Conclusion NAC and RvD1 may be exerted protective effect against oxidative stress on inflammatory response and mucus hypersecretion of DHBE by the activation of the NF-κB pathway.