Anti­inflammatory effects of 6­formyl umbelliferone via the NF­κB and ERK/MAPK pathway on LPS­stimulated RAW 264.7 cells.

Inhibition of over­activated inflammation has been demonstrated as one of the most efficient strategies for treating inflammatory diseases. In the present study, 6­formyl umbelliferone (6FU) was used to evaluate its anti­inflammatory effects on lipopolysaccharide (LPS)­stimulated RAW 264.7 macrophages. 6FU inhibited chronic inflammatory processes, including increasing nitric oxide levels, and the expression of pro­inflammatory genes and producing cytokines was investigated by a nitrite assay and reverse transcription­polymerase chain reaction, respectively. Nitric oxide and pro­inflammatory cytokines, including tumor necrosis factor­α, interleukin (IL)­1ß and IL­6 were decreased by treatment with 6FU, without cell cytotoxicity in LPS­stimulated RAW 264.7 cells, which was measured by a WST­1 assay. In the western blot analysis, the expression levels of phosphorylated extracellular signal­regulated kinase (ERK)1/2 was downregulated in 6FU­treated cells. Furthermore, in the western blotting and immunofluorescence staining results, translocation activities of ERK1/2 and NF­κB from the cytoplasm to the nucleus were suppressed, which may inhibit translation of numerous proteins associated with pro­inflammation, including inducible nitric oxide synthase and cyclooxygenase­2. Therefore, based on these results, it was suggested that 6FU may be a potential candidate for the development of agents against chronic inflammation.