ABSTRACT
[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-1βwere 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.