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Objective: Oxidative stress-mediated inflammatory events involve in the progress of several diseases such as asthma, cancers, and multiple sclerosis. Auraptene (AU), a natural prenyloxycoumarin, possesses numerous pharmacological activities. Here, the anti-inflammatory effects of AU were investigated in lipoteichoic acid- (LTA-) induced macrophage cells (RAW 264.7)., Methods: The expression of cyclooxygenase (COX-2), tumor necrosis factor (TNF- α ), interleukin-1 β (IL-1 β ), and inducible nitric oxide synthase (iNOS) and the phosphorylation of extracellular signal-regulated kinase (ERK) 1/2, p38 MAPK, c-Jun N-terminal kinase (JNK), heme oxygenase (HO-1), p65, and I κ B α were all identified by western blotting assay. The level of nitric oxide (NO) was measured by spectrometer analysis. The nuclear translocation of p65 nuclear factor kappa B (NF- κ B) was assessed by the confocal microscopic staining method. Native polyacrylamide gel electrophoresis was performed to perceive the activity of antioxidant enzyme catalase (CAT)., Results: AU expressively reduced NO production and COX-2, TNF- α , IL-1 β , and iNOS expression in LTA-stimulated cells. AU at higher concentration (10  µ M) inhibited ERK and JNK, but not p38 phosphorylation induced by LTA. Moreover, AU blocked I κ B and p65 phosphorylation, and p65 nuclear translocation. However, AU pretreatment was not effective on antioxidant HO-1 expression, CAT activity, and reduced glutathione (GSH, a nonenzymatic antioxidant), in LTA-induced RAW 264.7 cells., Conclusion: The findings of this study advocate that AU shows anti-inflammatory effects via reducing NF- κ B/MAPKs signaling pathways., Competing Interests: The authors declare no conflicts of interest., (Copyright © 2021 Chih-Hsuan Hsia et al.)