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)1β 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.