Background: The aim of this study was to investigate the levels of ROS and NO production and their related signal transduction by inflammatory status in macrophage. In this study, to investigate the Quercetin exerts its antioxidative action against oxidative stress and inflammation by suppressing the activation of the key pro-inflammatory transcriptional pathways, p38 MAPK and NF-觀B in macrophage. Methods Macrophage (Raw 264.7 cells) were cultured in RPMI-1640 containing 10% FBS, 2mM glutamine, 100 units/mL penicillin, and 100 關g/mL streptomycin at 37 C in a humidified atmosphere of 5% CO2 in air. Macrophages were plated at 90-95% confluence in all experiments. Nontoxic concentrations of Quercetin used in 24 h culture experiments were < 200 關M, as determined by the MTT assay. The intracellular generation of ROS was measured using carboxy-H2DCF-DA, a cell-permeable dye. Inside the cells, this compound is oxidized by ROS to form a fluorescent DCF. Briefly, cells seeded in 6-well plates at 1105 cells/well were treated with or without Quercetin and ROS inducer and then incubated with 10 關M carboxy-H2DCFDA at 37 C for 10 min. The cells were then washed twice with PBS. The rate of oxidation of the dye in the cells was monitored by flow cytometry. For signal transduction experiments, macrophage cells were lysed in an ice-cold and protein concentrations were measured using Bio-Rad colorimetric protein assay kits and performed Western blot. Results Quercetin significantly reduced ROS-induced inflammatory status in macrophage, as determined by cell ROS and NO generation, and inducible nitric oxide synthase expression. Moreover, pretreatment of macrophage with Quercetin also dose-dependently inhibited inflammatory chemokines production, indicating that it protects vascular against macrophage-induced ROS in atherosclerosis. Western blot analysis revealed that Quercetin also markedly inhibited several chemokines expression and suppressed both p38MAPK and NF-觀B activation in the ROS inducer -treated macrophage. Conclusion We demonstrated that the protective mechanisms underlying the actions of Quercetin against ROS inducer-induced ROS production in macrophage. These events are associated with ROS/NO scavenging and the inhibition of NF-B activation. Furthermore, these data should facilitate the informed use of Quercetin as an anti- atherosclerosis therapeutic adjuvant.