2-Bromo-5-Hydroxy-4-Methoxybenzaldehyde Suppresses the Activation of Inflammatory Mediators in LPS-Stimulated RAW 264.7 Cells

Abstract

In this study, we nvestigated the aility of 2-bromo-5-hydroxy-4-methoxybenzaldehyde (BMH) to inhibit lipopolysaccharide (LPS)-induced expressin of pro-inflammatory mediators in mouse macrophage (RAW 264.7) cells, and the molecular mechanism through which this inhibition occurred. Our results indicated that BHM downregulated LPS-induced nitric oxide (NO) synthase (iNOS) and cyclooxygenase-2 (COX-2) expression, thereby reducing the production of NO and prostaglanclin E2 (PGE2) in LPS-activated RAW 264.7 cells. Furthermore, BHM suppressed LPS-induced production of pro-inflammatory cytokines such as interleukin (IL)-1β, IL-6, and tumor necrosis factor (TN F)-α. In addition, BHM inhibited the activation of NF-кB and mitogen-activated protein kianses (MAPKs) pathways in a concentration-dependent manner. These results indicate that BHM inhibits LPS-stimuated inflammation by inhibition of the NF-кB and MAPKs pathways in macrophages. through which this inhibition occurred. Our results indicated that BHM downregulated LPS-induced nitric oxide (NO) synthase (iNOS) and cyclooxygenase-2 (COX-2) expression, thereby reducing the production of NO and prostaglanclin E2 (PGE2) in LPS-activated RAW 264.7 cells. Furthermore, BHM suppressed LPS-induced production of pro-inflammatory cytokines such as interleukin (IL)-1β, IL-6, and tumor necrosis factor (TN F)-α. In addition, BHM inhibited the activation of NF-кB and mitogen-activated protein kianses (MAPKs) pathways in a concentration-dependent manner. These results indicate that BHM inhibits LPS-stimuated inflammation by inhibition of the NF-кB and MAPKs pathways in macrophages.