Anti-inflammatory effects of 6-formyl umbelliferone via the NF-[kappa]B and ERK/MAPK pathway on LPS-stimulated RAW 264.7 cells

Inhibition of over-activated inflammation has been demonstrated as one of the most efficient strategies for treating inflammatory diseases. In the present study, 6-formyl umbelliferone (6FU) was used to evaluate its anti-inflammatory effects on lipopolysaccharide (LPS)-stimulated RAW 264.7 macrophages. 6FU inhibited chronic inflammatory processes, including increasing nitric oxide levels, and the expression of pro-inflammatory genes and producing cytokines was investigated by a nitrite assay and reverse transcription-polymerase chain reaction, respectively. Nitric oxide and pro-inflammatory cytokines, including tumor necrosis factor-[alpha], interleukin (IL)-1[beta] and IL-6 were decreased by treatment with 6FU, without cell cytotoxicity in LPS-stimulated RAW 264.7 cells, which was measured by a WST-1 assay. In the western blot analysis, the expression levels of phosphorylated extracellular signal-regulated kinase (ERK)l/2 was downregulated in 6FU-treated cells. Furthermore, in the western blotting and immunofluorescence staining results, translocation activities of ERK1/2 and NF-[kappa]B from the cytoplasm to the nucleus were suppressed, which may inhibit translation of numerous proteins associated with pro-inflammation, including inducible nitric oxide synthase and cyclooxygenase-2. Therefore, based on these results, it was suggested that 6FU may be a potential candidate for the development of agents against chronic inflammation.