【Objective】To investigate the pharmacological mechanism of montelukast in the inhibition of inflammation.【Meth? ods】Respiratory syncytial virus-infected human bronchial epithelial cell（16HBEC）inflammatory cell model was established，and mRNA and protein expressions of Nuclear factor NF-E2 related factor（Nrf2），heme oxygenase（HO-1），quinone oxidoreductase （NQO-1），and glutathione transferase（GST）were determined by qPCR and Western-blot，and production of cellular reactive oxygen species（ROS）was measured by DCFH-DA fluorescent probe method. Nrf2 siRNA was further synthesized to reduce the expression of Nrf2，to investigate the chang of inflammatory index.【Results】Montelukast significantly reduced the expressions of inflammatory cytokines IL-6，TNF-α，and IL-1β（P < 0.05）on respiratory syncytial virus-infected 16HBEC，and the ROS level in inflammatory cell model was decreased（P < 0.05），increased the mRNA and protein expressions of Nrf2，HO-1，NQO-1 and GST （P < 0.05），with a more significant effect at higher dose. After the down-regulation of Nrf2，the expressions of inflammatory cyto? kines IL-6，TNF-α，and IL-1β were increased（P < 0.05），and ROS level was significantly increased（P < 0.05），mRNA and pro? tein expressions of Nrf2，HO-1，NQO-1 and GST were decreased（P < 0.05）.【Conclusion】Montelukast inhibits the inflammation of human bronchial epithelial cells infected by respiratory syncytial virus（RSV），and the potential mechanism may involve its ef? fect on the Nrf2/ARE signaling pathway.