TY - JOUR
T1 - Anti-inflammatory effects of 6-formyl umbelliferone via the NF-?B and ERK/MAPK pathway on LPS-stimulated RAW 264.7 cells
AU - Kim, Sangbo
AU - Kang, Minjae
AU - Kang, Changwon
AU - Kim, Nanhee
AU - Choi, Hyung Wook
AU - Jung, Hyun Ah
AU - Choi, Jae Sue
AU - Kim, Gundo
N1 - Publisher Copyright:
© 2019 Spandidos Publications. All Rights Reserved.
PY - 2019/4
Y1 - 2019/4
N2 - 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-a, interleukin (IL)-1ß a nd I L-6 were d ecreased by t reatment w ith 6 FU, 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)1/2 was downregulated in 6FU-treated cells. Furthermore, in the western blotting and immunofluorescence staining results, translocation activities of ERK1/2 and NF-?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.
AB - 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-a, interleukin (IL)-1ß a nd I L-6 were d ecreased by t reatment w ith 6 FU, 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)1/2 was downregulated in 6FU-treated cells. Furthermore, in the western blotting and immunofluorescence staining results, translocation activities of ERK1/2 and NF-?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.
KW - 6formyl umbelliferone
KW - Anti-inflammation
KW - COX-2
KW - NF-?B
KW - iNOS
UR - http://www.scopus.com/inward/record.url?scp=85062440714&partnerID=8YFLogxK
U2 - 10.3892/ijmm.2019.4078
DO - 10.3892/ijmm.2019.4078
M3 - Article
SN - 1107-3756
VL - 43
SP - 1859
EP - 1865
JO - International Journal of Molecular Medicine
JF - International Journal of Molecular Medicine
IS - 4
ER -